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1.
Summary Alpha-smooth muscle actin is currently considered a marker of smooth muscle cell differentiation. However, during various
physiologic and pathologic conditions, it can be expressed, sometimes only transiently, in a variety of other cell types,
such as cardiac and skeletal muscle cells, as well as in nonmuscle cells. In this report, the expression of actin mRNAs in
cultured rat capillary endothelial cells (RFCs) and aortic smooth muscle cells (SMCs) has been studied by Northern hybridization
in two-dimensional cultures seeded on individual extracellular matrix proteins and in three-dimensional type I collagen gels.
In two-dimensional cultures, in addition to cytoplasmic actin mRNAs which are normally found in endothelial cell populations,
RFCs expressed α-smooth muscle (SM) actin mRNA at low levels. α-SM actin mRNA expression is dramatically enhanced by TGF-β1. In addition, double immunofluorescence staining with anti-vWF and anti-α-SM-1 (a monoclonal antibody to α-SM actin) shows
that RFCs co-express the two proteins. In three dimensional cultures, RFCs still expressed vWF, but lost staining for α-SM
actin, whereas α-SM actin mRNA became barely detectable. In contrast to two-dimensional cultures, the addition of TGF-β1 to the culture media did not enhance α-SM actin mRNA in three-dimensional cultures, whereas it induced rapid capillary tube
formation. Actin mRNA expression was modulated in SMCs by extracellular matrix components and TGF-β1 with a pattern very different from that of RFCs. Namely, the comparison of RFCs with other cell types such as bovine aortic
endothelial cells shows that co-expression of endothelial and smooth muscle cell markers is very unique to RFCs and occurs
only in particular culture conditions. This could be related to the capacity of these microvascular endothelial cells to modulate
their phenotype in physiologic and pathologic conditions, particularly during angiogenesis, and could reflect different embryologic
origins for endothelial cell populations.
Supported by a Post-Doctoral Fellowship from the Swiss National Science Foundation (OK) and grant HL-RO1-28373 (JAM) from
the Department of Human Services, Public Health Service, Washington, D.C. 相似文献
2.
Yamada M Kuwano K Maeyama T Hamada N Yoshimi M Nakanishi Y Kasper M 《Histochemistry and cell biology》2008,129(4):453-462
epithelial–mesenchymal transition (EMT) has been considered to be involved in organ fibrogenesis. However, there is few direct
evidence of this process in the pathophysiology of pulmonary fibrosis in vivo. Therefore, we tried to verify the involvement
of this process in the development of pulmonary fibrosis. Since the co-expressions of epithelial and mesenchymal markers are
thought to be a marker of EMT, we performed dual-immuunohistochemistry to assess the co-expressions of these proteins in lung
tissues from bleomycin-induced pulmonary fibrosis in mice, and from patients with idiopathic pulmonary fibrosis, and nonspecific
interstitial pneumonia. Double positive cells for epithelial markers including E-cadherin, T1α, or aquaporin 5, and a mesenchymal
markers α-smooth muscle actin or vimentin were not found in bleomycin-induced pulmonary fibrosis in mice. Double positive
cells for E-cadherin, ICAM-1, LEA, CD44v9, or SP-A and α-smooth muscle actin or vimentin were not found in lung tissues from
normal lung parenchyma, idiopathic pulmonary fibrosis and nonspecific interstitial pneumonia. These results offer at least
two possibilities. One is that EMT does not occur in IPF or bleomycin-induced pulmonary fibrosis in mice. Another is that
EMT may occur in pulmonary fibrosis but the time during this transition in which cells express detectable levels of epithelial
and mesenchymal markers is too small to be detected by double immunohistochemistry. 相似文献
3.
L. I. Khozhai V. A. Otellin K. M. Pozharisskii N. G. Pavlova 《Journal of Evolutionary Biochemistry and Physiology》2010,46(3):275-281
Changes of expression of contractile proteins (smooth muscle cell α-actin and myosin) and of type IV collagen in villous stroma
of human placenta were studied at the diagnosed placental insufficiency (PI) in III trimester of pregnancy. The study revealed
pronounced disturbances of expression of contractile proteins and type IV collagen at PI. It is shown that in perivascular
sheaths of vessels of stem and intermediate villi there is present a much greater amount of cells expressing smooth muscle
actin and myosin. These cells are arranged by the denser concentric layers and more compactly than in norm and fill the intervascular
space inside the villi. The width of perivascular sheaths of vessels is higher, while vascular lumens are lower than in norm.
In terminal villi the capillary walls are thickened and the number of pericytes immunopositive against the smooth muscle cell
α-actin and myosin as well as type IV collagen is increased. The change of synthesis of the cytoskeletal contractile proteins
and type IV collagen is shown to lead to structural disturbances of villi of different types and of perivascular areas and
vessels, which doubtlessly indicates their participation in pathogenesis of placental dysfunction and of disturbance of placental
hemodynamics. 相似文献
4.
Daniele Brouty-Boye Despina Kolonias Niramol Savaraj Theodore J. Lampidis 《In vitro cellular & developmental biology. Animal》1992,28(4):293-296
Summary Using a panel of monoclonal anitbodies to several different cytoskeletal elements in primary cultures derived from newborn
rat hearts we report that fibroblasts similar to cardiac-muscle cells expressed theα-actin isoform of smooth muscle cells. However, striated muscleα-actin or desmin antibodies did not stain cardiac fibroblasts but did stain cardiac-muscle cells. Theα-smooth muscle actin distributed as a stress fiber and in a cross-striated pattern in cardiac muscle while fibroblasts showed
exclusive stress fiber staining. These results suggest that connective tissue cells during development of the heart contain
muscle-specific elements which may relate to the organ-specific contractile function with which they are associated. 相似文献
5.
This study was carried out to determine whether sympathectomy influences the phenotypic modulation of smooth muscle cells
in the peripheral and cerebral arteries of heritable hyperlipidaemic rabbits. Unilateral superior cervical ganglionectomy
(common origin of innervation to the middle cerebral artery and the central ear artery) was performed on four Watanabe heritable
hyperlipidaemic rabbits. Cross-sections of the ipsi- (sympathectomized) and the contralateral (intact) cerebral and ear arteries
were prepared 2 months later and labelled with monoclonal antibodies against vimentin and desmin, two markers of the differentiation
of smooth muscle cells, and α-smooth muscle actin, a marker of these cells. Sections from control and sympathectomized arteries
were analysed with a confocal laser scanning microscope. Compared with contralateral intact ear arteries, the sympathectomized
ear artery developed a thickened intima with dedifferentiated smooth muscle cells, expressing α-smooth muscle actin but no
desmin, whereas the middle cerebral artery remained unchanged. These results suggest that sympathectomy may favour the progression
of atherosclerosis in peripheral but not in cerebral arteries of Watanabe heritable hyperlipidaemic rabbits 相似文献
6.
Lone Rønnov-Jessen Bo van Deurs Maja Nielsen Ole W. Petersen 《In vitro cellular & developmental biology. Animal》1992,28(4):273-283
Summary Myofibroblasts from human breast carcinomas were identified and experimentally generated in culture, and a possible function
was examined. The frequency ofα-smooth muscle actin immunoreactive cells was evaluated as a measure of myofibroblast differentiation in primary culture.
Few or noα-smooth muscle actin-positive stromal cells (6.1 ± 8.4%) were identified in primary cultures from normal breast tissue (n=9). In contrast, high frequencies (68.8 ± 15.1%) were observed in primary cultures from carcinomas (n=19). The frequencies of myofibroblasts in primary cultures were almost identical to those obtained in the corresponding cryostat
sections (69.1 vs. 68.8%). A possible precursor cell to the myofibroblast was looked for among typical fibroblasts and vascular
smooth muscle cells. Purified blood vessels containing both fibroblasts and vascular smooth muscle cells were embedded in
collagen gel and incubated with medium conditioned by breast epithelial cells. Fibroblasts rather than smooth muscle cells
were recruited from the blood vessels. In medium conditioned by carcinoma cell lines or in co-cultures of carcinoma cell lines
and purified fibroblasts,α-smooth muscle actin and the typical myofibroblast phenotype were induced in otherwiseα-smooth muscle actin-negative fibroblasts. The effect of myofibroblasts on cellular movement—essential to neoplastic cells—was
analyzed. Spontaneous motility of tumor cells (MCF-7) was entirely suppressed in a collagen gel assay. Under these conditions
tumor cell motility was selectively mediated by direct cell-to-cell interaction between tumor cells and myofibroblasts. Under
chemically defined conditions, interaction was dependent on the presence of plasminogen. Anti-plasminogen, soybean trypsin
inhibitor, and anti-fibronectin partly neutralized the effect of plasminogen. It is concluded that elements of myofibroblast
differentiation and function may be studied in culture. 相似文献
7.
Immunohistochemistry of -smooth muscle actin and desmin, two markers of smooth muscle cell differentiation, and electron-microscopic observation of thick filaments of myosin were performed on the media of the developing rat hepatic portal vein to gain insights into the chronology of differentiation of its longitudinal and circular smooth muscles. In accordance with the ultrastructural distribution of thin filaments, staining of -smooth muscle actin is lightly positive in the myoblasts at postnatal day 1 and then extends in probably all muscle cells of the developing vessel. Desmin, which appears later than -smooth muscle actin in the two muscles, is distributed throughout the longitudinal layer at day 8, whereas the first arrangements of thick filaments are detectable in most longitudinal muscle cells; at this stage, desmin and thick filaments are absent from the poorly differentiated circular muscle cells. The longitudinal muscle cells differentiate in a strikingly synchronized way from day 8 onwards, conferring a homogeneous structure to the developing and mature longitudinal layer. Several desmin-positive cells and a heterogeneous distribution of thick filaments occur in the circular muscle at day 14; the subsequent extension of these filaments in this layer results in a persisting heterogeneous distribution in the young 7-week-old adult. Many features of the mature smooth muscle cells are established within the third week in the longitudinal muscle, approximately one week before those of the circular layer. These results are consistent with the function of the longitudinal muscle as a spontaneously contractile smooth muscle unit, and emphasize the need for its fast maturation to fulfil its major role in the control of portal blood flow. 相似文献
8.
Rishikof DC Lucey EC Kuang PP Snider GL Goldstein RH 《Histochemistry and cell biology》2006,125(5):527-534
The repair of alveolar structures following endotracheal administration of porcine pancreatic elastase (PPE) to mice involves the coordinated deposition of new matrix elements. We determined the induction of the myofibroblast phenotype following elastolytic injury to mouse lung by examining the expression of α-smooth muscle actin (α-SMA) by immunohistochemistry. We also examined elastin and α1(I) collagen mRNA expression by in situ hybridization. Changes in airspace dimensions were assessed by determining mean linear intercept. In untreated mice, α-SMA was localized to vascular structures and large airways, with no detectable expression in alveolar units. PPE induced α-SMA expression in damaged areas surrounding large vessels, in septal remnants, and in the opening ring of alveolar ducts. Elastin and α1(I) collagen mRNA expression were up-regulated in residual alveolar structures and septal walls. PPE dose-response studies indicated that α1(I) collagen and elastin mRNA expression were not induced in areas of normal lung adjacent to damaged lung. The administration of low dose PPE resulted in increased α-SMA protein and elastin mRNA expression in the cells comprising the opening ring of alveolar ducts. Our data suggest that repair mechanisms following elastolytic injury are confined to overtly damaged alveolar structures and involve the induction of the myofibroblast phenotype. 相似文献
9.
Wanda Durand-Arczynska Nelly Marmy Jacques Durand 《Histochemistry and cell biology》1993,100(6):465-471
Calponin and caldesmon are two proteins considered to play a regulatory role in smooth muscle contraction, which have never previously been found to be expressed in subcultured cells. In the present study, immunocytochemistry and immunoblotting were performed to identify these proteins in smooth muscle cells (SMC) from human bronchi. It was found that human airway SMC, kept in a non-proliferative state, continued to express caldesmon and calponin at least until the 8th passage. The expression of -smooth muscle actin studied under the same conditions was also shown to be preserved in subcultured bronchial SMC. 相似文献
10.
11.
Christine Galustian Julian Dye Lopa Leach Peter Clark J. Anthony Firth 《In vitro cellular & developmental biology. Animal》1995,31(10):796-802
Summary The microfilamentous actin component of the cytoskeleton is crucial to endothelial angiogenesis and vascular permeability.
Differences in actin cytoskeletal profiles in cultured human endothelial cells were explored: when first isolated, both primary
human umbilical vein endothelial cells (HUVEC) and primary human placental microvascular endothelial cells (HPMEC) expressed
F-actin, but notβ-actin orα-smooth muscle actin. A similar endothelial actin profile was observed in cryo-sections of freshly delivered term umbilical
cord and placenta. In subsequent cell culture, although the actin cytoskeleton of HUVEC remained unchanged, the actin profiles
of HPMEC altered after the second passage with the induction ofα-smooth muscle actin expression, which was intercellularly heterogeneous and increased to 20% at P4. This behavior occurred
in HPMEC monolayers cultured on a variety of extracellular matrices. Comparisons with a spontaneously immortalized human microvascular
cell-line, HGTEN 21, revealed that inprolonged passage, bothα-smooth muscle actin andβ-actin were expressed, whereas HPMEC at P4 showed a lower level ofβ-actin expression. Therefore, in comparison with large vessels, microvascular cells are more likely to dedifferentiate. This
may reflect the ability of microvascular cells to remodel according to changing requirement for new vessel formation. In conclusion,
passage of human microvascular endothelial cells, but not of larger vessel endothelial cells, alters the expression of actin
isoforms. This may be important in relation to comparisons ofin vitro andin vivo vascular permeability; higher passage microvascular endothelial cells should thus be used with caution in such studies. 相似文献
12.
《生物化学与生物物理学报:疾病的分子基础》2007,1772(11-12):1250-1257
13.
Martha S. Lundberg Devaki N. Sadhu Vicky E. Grumman William M. Chilian Kenneth S. Ramos 《In vitro cellular & developmental biology. Animal》1995,31(8):595-600
Summary The occurrence of vascular domains with specific biological and pharmacological characteristics suggests that smooth muscle
cells in different arteries may respond differentially to a wide range of environmental stimuli. To determine if some of these
vessel-specific differences may be attributable to mechano-sensitive gene regulation, the influence of cyclical stretch on
the expression of actin isoform and α1B-adrenoceptor genes was examined in aortic and coronary smooth muscle cells. Cells were seeded on an elastin substrate and
subjected to maximal stretching (24% elongation) and relaxation cycles at a frequency of 120 cycles/min in a Flexercell strain
unit for 72 h. Total RNA was extracted and hybridized to radiolabeled cDNA probes to assess gene expression. Stretch caused
a greater reduction of actin isoform mRNA levels in aortic smooth muscle cells as compared to cells from the coronary artery.
Steady-state mRNA levels of α1B -adrenoceptor were also decreased by cyclical stretch in both cell types but the magnitude of the response was greater in
coronary smooth muscle cells. No changes in α1B-adrenoceptor or β/γ-actin steady-state mRNA levels were observed in H4IIE cells, a nonvascular, immortalized cell line. The
relative gene expression of heat shock protein 70 was not influenced by the cyclic stretch regimen in any of these cell types.
These results suggest that stretch may participate in the regulation of gene expression in vascular smooth muscle cells and
that this response exhibits some degree of cell-specificity. 相似文献
14.
The present study demonstrates histological and immunohistochemical changes in the peritubular testicular tissue of rat testis
after application of cadmium chloride. After 5-day cadmium exposure, advanced deterioration of the boundary testicular tissue,
mainly oedema, disarrangement of collagen fibres and peritubular cells, dilatation and thrombosis of blood vessels were observed.
Changes in the boundary tissue were accompanied with desquamation of the germinal epithelium. Immunohistochemically, positive
reaction for α-smooth muscle actin and desmin in tunica media of large testicular blood vessels basically was not affected.
No reaction for vimentin was seen in endothelial cells of blood capillaries, whereas positive reaction presented only these
cells in large blood vessels. The myofibroblasts positively reacting for desmin and α-smooth muscle actin form a single incomplete
layer in the lamina propria of seminiferous tubules. Vimentin reactivity in the myofibroblasts and in the supporting Sertoli
cells as well as Leydig cells in damaged testicular tissue was not observed. An increase in fibroblasts and free inflammatory
cells positive for vimentin in the peritubular space on the peripheric area of the testis was observed. 相似文献
15.
Myoepithelial molecular markers in human breast carcinoma PMC42-LA cells are induced by extracellular matrix and stromal cells 总被引:3,自引:0,他引:3
Lebret SC Newgreen DF Waltham MC Price JT Thompson EW Ackland ML 《In vitro cellular & developmental biology. Animal》2006,42(10):298-307
Summary The microenvironment plays a key role in the cellular differentiation of the two main cell lineages of the human breast, luminal
epithelial, and myoepithelial. It is not clear, however, how the components of the microenvironment control the development
of these cell lineages. To investigate how lineage development is regulated by 3-D culture and microenvironment components,
we used the PMC42-LA human breast carcinoma cell line, which possesses stem cell characteristics. When cultured on a two-dimensional
glass substrate, PMC42-LA cells formed a monolayer and expressed predominantly luminal epithelial markers, including cytokeratins
8, 18, and 19; E-cadherin; and sialomucin. The key myoepithelial-specific proteins α-smooth muscle actin and cytokeratin 14
were not expressed. When cultured within Engelbreth-Holm-Swarm sarcoma-derived basement membrane matrix (EHS matrix), PMC42-LA
cells formed organoids in which the expression of luminal markers was reduced and the expression of other myoepithelial-specific
markers (cytokeratin 17 and P-cadherin) was promoted. The presence of primary human mammary gland fibroblasts within the EHS
matrix induced expression of the key myoepithelial-specific markers, α-smooth muscle actin and cytokeratin 14. Immortalized
human skin fibroblasts were less effective in inducing expression of these key myoepithelial-specific markers. Confocal dual-labeling
showed that individual cells expressed luminal or myoepithelial proteins, but not both. Conditioned medium from the mammary
fibroblasts was equally effective in inducing myoepithelial marker expression. The results indicate that the myoepithelial
lineage is promoted by the extracellular matrix, in conjunction with products secreted by breast-specific fibroblasts. Our
results demonstrate a key role for the breast microenvironment in the regulation of breast lineage development. 相似文献
16.
Nair DG Han TY Lourenssen S Blennerhassett MG 《American journal of physiology. Gastrointestinal and liver physiology》2011,300(5):G903-G913
Intestinal inflammation causes an increased intestinal wall thickness, in part, due to the proliferation of smooth muscle cells, which impairs the contractile phenotype elsewhere. To study this, cells from the circular muscle layer of the rat colon (CSMC) were isolated and studied, both in primary culture and after extended passage, using quantitative PCR, Western blot analysis, and immunocytochemistry. By 4 days in vitro, both mRNA and protein for the smooth muscle marker proteins α-smooth muscle actin, desmin, and SM22-α were reduced by >50%, and mRNA for cyclin D1 was increased threefold, evidence for modulation to a proliferative phenotype. Continued growth caused significant further decrease in expression, evidence that phenotypic loss in CSMC was proportional to the extent of proliferation. In CSMC isolated at day 2 of trinitrobenzene sulfonic acid-induced colitis, flow cytometry and Western blotting showed that these differentiated markers were reduced in mitotic CSMC, while similar to control in nonmitotic CSMC. By day 35 post-trinitrobenzene sulfonic acid, when inflammation has resolved, CSMC were hypertrophic, but, nonetheless, showed markedly decreased expression of smooth muscle protein markers per cell. In vitro, day 35 CSMC displayed an accelerated loss of phenotype and increased thymidine uptake in response to serum or PDGF-BB. Furthermore, carbachol-induced expression of phospho-AKT (a marker of cholinergic response) was lost from day 35 CSMC in vitro, while retained in control cells. Therefore, proliferation reduces the expression of smooth-muscle-specific markers in CSMC, possibly leading to altered contractility. However, inflammation-induced proliferation in vivo also causes lasting changes that include unexpected priming for an exaggerated response to proliferative stimuli. Identification of the molecular mechanisms of intestinal smooth muscle cell phenotypic modulation will be helpful in reducing the detrimental effects of inflammation. 相似文献
17.
Gaby Kohnen Sonja Kertschanska Ramazan Demir Peter Kaufmann 《Histochemistry and cell biology》1996,105(6):415-429
Different subtypes of myofibroblasts have been described according to their cytoskeletal protein patterns. It is quite likely that these different subtypes represent distinct steps of differentiation. We propose the human placental stem villi as a particularly suitable model to study this differentiation process. During the course of pregnancy, different types of placental villi develop by differentiation of the mesenchymal stroma surrounding the fetal blood vessels. In order to characterise the differentiation of placental stromal cells in the human placenta, the expression patterns of the cytoskeletal proteins vimentin, desmin, - and -smooth muscle actin, pan-actin, smooth muscle myosin, and the monoclonal antibody GB 42, a marker of myofibroblasts, were investigated on placental tissue of different gestational age (7th–40th week of gestation). Proliferation patterns were assessed with the proliferation markers MIB 1 and PCNA. Additionally, dipeptidyl peptidase IV distribution was studied in term placenta and the ultrastructure of placental stromal cells was assessed by electron microscopy. Different subpopulations of extravascular stromal cells were distinguished according to typical co-expression patterns of cytoskeletal proteins. Around the fetal stem vessels in term placental villi they were arranged as concentric layers with increasing stage of differentiation. A variable layer of extravascular stromal cells lying beneath the trophoblast expressed vimentin (V) or vimentin and desmin (VD). They were mitotically active. The next layer co-expressed vimentin, desmin, and -smooth muscle actin (VDA). More centrally towards the fetal vessels, extravascular stromal cells co-expressed vimentin, desmin, - and -smooth muscle actin, and GB 42 (VDAG). Cells close to the fetal vessels additionally co-expressed smooth muscle myosin (VDAGM). Ultrastructurally, V cells resembled typical mesenchymal cells. VD cells corresponded to fibroblasts, while VDA and VDAG cells developed features of myofibroblasts. Cells of the VDAGM-type revealed a smooth muscle cell-related ultrastructure. In earlier stages of pregnancy, stromal cell types with less complex expression patterns prevailed. The media smooth muscle cells of the fetal vessels showed a mixture of different co-expression patterns. These cells were separated from extravascular stromal cells by a layer of collagen fibres. The results obtained indicate a clearly defined spatial differentiation gradient with increasing cytoskeletal complexity in human placental stromal cells from the superficial trophoblast towards the blood vessels in the centre of the stem villi. The spatial distribution of the various stages of differentiation suggests that human placental villi could be a useful model for the study of the differentiation of myofibroblasts. 相似文献
18.
Annette Schmitt-Gräff Omar Skalli Giulio Gabbiani 《Virchows Archiv. B, Cell pathology including molecular pathology》1989,57(1):291-302
A series of 217 trephine bone marrow biopsies from adult patients and specimens from 16 fetuses and 5 infants were examined
for the presence of stromal myoid cells (MCs) using a monoclonal antibody recognizing α-smooth muscle actin. In the normal
adult bone marrow, stromal cells did not contain α-smooth muscle actin, whereas during fetal life, many α-smooth muscle actin-containing
MCs were connected with vascular sinusoids in the primitive bone marrow. This cell type reappeared in various characteristic
distribution patterns in adult bone marrow during different neoplastic and non-neoplastic conditions including metastatic
carcinoma, Hodgkin’s disease, multiple myeloma, hairy cell leukemia, acute myeloid leukemia (FAB M4, 5, 7) and chronic myeloproliferative
diseases. In general, the appearance of MCs was associated with a slight to pronounced increase in the deposition of reticulin
and collagen fibers. We propose that bone marrow MCs represent a distinct subpopulation of fiber-associated or adventitial
reticular cells undergoing cytoskeletal remodeling in response to various stimuli. 相似文献
19.
Tang DD Tan J 《American journal of physiology. Heart and circulatory physiology》2003,285(4):H1528-H1536
The actin-regulatory protein profilin has been shown to regulate the actin cytoskeleton and the motility of nonmuscle cells. To test the hypothesis that profilin plays a role in regulating smooth muscle contraction, profilin antisense or sense oligodeoxynucleotides were introduced into the canine carotid smooth muscle by a method of reversible permeabilization, and these strips were incubated for 2 days for protein downregulation. The treatment of smooth muscle strips with profilin antisense oligodeoxynucleotides inhibited the expression of profilin; it did not influence the expression of actin, myosin heavy chain, and metavinculin/vinculin. Profilin sense did not affect the expression of these proteins in smooth muscle tissues. Force generation in response to stimulation with norepinephrine or KCl was significantly lower in profilin antisense-treated muscle strips than in profilin sense-treated strips or in muscle strips not treated with oligodeoxynucleotides. The depletion of profilin did not attenuate increases in phosphorylation of the 20-kDa regulatory light chain of myosin (MLC20) in response to stimulation with norepinephrine or KCl. The increase in F-actin/G-actin ratio during contractile stimulation was significantly inhibited in profilin-deficient smooth muscle strips. These results suggest that profilin is a necessary molecule of signaling cascades that regulate carotid smooth muscle contraction, but that it does not modulate MLC20 phosphorylation during contractile stimulation. Profilin may play a role in the regulation of actin polymerization or organization in response to contractile stimulation of smooth muscle. 相似文献