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1.
P. Hiscott H. A. Waller I. Grierson M. G. Butler D. Scott 《Cell and tissue research》1992,267(1):185-192
Summary The distribution of fibronectin mRNA and fibronectin in adult human retina and epiretinal membranes was investigated by in situ hybridisation and immunohistochemical techniques. The cells in normal adult retina contained little or no fibronectin mRNA and the retina only showed fibronectin immunoreactivity in retinal vessels. The cells in detached neuroretina did not contain fibronectin message but the vitreoretinal interface of the detached retina exhibited variable fibronectin immunoreactivity. Retinal glia, retinal pigment epithelium and fibroblast-like cells in membranes at the vitreoretinal juncture (epiretinal membranes) showed variable labelling with the fibronectin mRNA probe and all the membranes immunostained for fibronectin. No difference could be detected between membrane cell types in the intensity of labelling with the mRNA probe or for fibronectin immunoreactivity. The results indicate that cells in situ in attached and detached adult human retina do not produce fibronectin. Although fibronectin at the vitreoretinal juncture in retinal detachment is probably partly derived from plasma fibronectin resulting from breakdown of the blood-retinal barrier, ectopic retinal cells produce fibronectin and contribute to the glycoprotein in epiretinal membranes. 相似文献
2.
Summary We have mapped the regions of young leaves from 2-, 3-, and 4-week-old axenically grownZea mays L. cv. Seneca 60 plants capable of proliferation in culture. The capacity of 3 mm wide segments to form proliferating cultures was limited to a zone within the first approximately 40 mm from the leaf base independent of leaf length. Within this zone the incidence of forming proliferating cultures was constant. The responsive zones were found in pairs of adjacent leaves: leaf 3 and 4 at 2 weeks, leaf 4 and 5 at 3 weeks, and leaf 5 and 6 at 4 weeks. We conclude that there is a window of proliferative potential with definite boundaries. This window appears to move toward developmentally younger pairs of leaves with increasing age of the plant. 相似文献
3.
Toshitsugu Nakamura Masao Hotchi 《Virchows Archiv. B, Cell pathology including molecular pathology》1993,63(1):11-16
DNA strand breaks (nicks) in non-parenchymal cells (NPCs) in CCl4-induced acute or chronic liver injury in rats were detected using an in situ nick translation method; their dynamic changes
were analysed in relation to the proliferation pattern of hepatocytes and NPCs, as revealed by bromodeoxyuridine (BrdU)-up-take.
In acute injury, hepatocyte proliferation started before centrilobular necrosis had occurred, whereas BrdU-labeled sinusoidal
NPCs markedly increased only after centrilobular necrosis was apparent. DNA breakages in NPCs paralleled the proliferation
pattern of these cells, suggesting that nicks are physiological, and reflect proliferation and activated gene expression.
In chronic injury, liver cirrhosis developed after 9 weeks, but BrdU-labeling of hepatocytes was almost the same level as
that in untreated liver. The number of BrdU-labeled NPCs showed only a slight increase, while those with DNA breakages were
much more frequent in the cirrhotic stage, suggesting a significant role for NPCs in the fibrotic process. These results indicate
that DNA strand breaks in NPCs act as a marker for activation states such as proliferation, differentiation and/or activated
gene expression. 相似文献
4.
Xuebin Yu Qiufeng Teng Kaimin Bao Maryam Chudhary Hui Qi Wenying Zhou Hongxin Che Junli Liu Xiang Ren Li Kong 《Journal of cellular biochemistry》2023,124(3):421-433
As one of the common and serious chronic complications of diabetes mellitus (DM), the related mechanism of diabetic retinopathy (DR) has not been fully understood. Müller cell reactive gliosis is one of the early pathophysiological features of DR. Therefore, exploring the manner to reduce diabetes-induced Müller cell damage is essential to delay DR. Thioredoxin 1 (Trx1), one of the ubiquitous redox enzymes, plays a vital role in redox homeostasis via protein–protein interactions, including apoptosis signal-regulating kinase 1 (ASK1). Previous studies have shown that upregulation of Trx by some drugs can attenuate endoplasmic reticulum stress (ERS) in DR, but the related mechanism was unclear. In this study, we used DM mouse and high glucose (HG)-cultured human Müller cells as models to clarify the effect of Trx1 on ERS and the underlying mechanism. The data showed that the diabetes-induced Müller cell damage was increased significantly. Moreover, the expression of ERS and reactive gliosis was also upregulated in diabetes in vivo and in vitro. However, it was reversed after Trx1 overexpression. Besides, ERS-related protein expression, reactive gliosis, and apoptosis were decreased after transfection with ASK1 small-interfering RNA in stable Trx1 overexpression Müller cells after HG treatment. Taken together, Trx1 could protect Müller cells from diabetes-induced damage, and the underlying mechanism was related to inhibited ERS via ASK1. 相似文献
5.
BackgroundGluconeogenesis and renal glucose excretion in kidneys both play an important role in glucose homeostasis. Sodium-glucose cotransporter (SGLT2), coded by the SLC5A2 gene is responsible for reabsorption up to 99% of the filtered glucose in proximal tubules. SLC5A2 genetic polymorphisms were suggested to influence glucose homeostasis. We investigated if common SLC5A2 rs9934336 polymorphism influences glycemic control and risk for macro or microvascular complications in Slovenian type 2 diabetes (T2D) patients.MethodsAll 181 clinically well characterized T2D patients were genotyped for SLC5A2 rs9934336 G>A polymorphism. Associations with glycemic control and T2D complications were assessed with nonparametric tests and logistic regression.ResultsSLC5A2 rs9934336 was significantly associated with increased fasting blood glucose levels (P<0.001) and HbA1c levels under the dominant genetic model (P=0.030). After adjustment for T2D duration, significantly higher risk for diabetic retinopathy was present in carriers of at least one polymorphic SLC5A2 rs9934336 A allele compared to non-carriers (OR=7.62; 95%CI=1.65-35.28; P=0.009).ConclusionsOur pilot study suggests an important role of SLC5A2 polymorphisms in the physiologic process of glucose reabsorption in kidneys in T2D patients. This is also the first report on the association between SLC5A2 polymorphism and diabetic retinopathy. 相似文献
6.
I-Hui Yang Yao-Ting Tsai Siou-Jin Chiu Li-Teh Liu Hsuan-Hung Lee Ming-Feng Hou Wen-Li Hsu Ben-Kuen Chen Wei-Chiao Chang 《Journal of biomedical science》2013,20(1):41
Background
In non-excitable cells, one major route for calcium entry is through store-operated calcium (SOC) channels in the plasma membrane. These channels are activated by the emptying of intracellular Ca2+ store. STIM1 and Orai1 are major regulators of SOC channels. In this study, we explored the functions of STIM1 and Orai1 in epidermal growth factor (EGF)-induced cell proliferation and migration in retinal pigment epithelial cells (ARPE-19 cell line).Results
EGF triggers cell proliferation and migration in ARPE-19 cells. Cell proliferation and migration involve STIM1 and Orai1, as well as phosphorylation of extracellular signal-regulated protein kinase (ERK) 1/2, and Akt. Pharmacological inhibitors of SOC channels and siRNA of Orai1 and STIM1 suppress cell proliferation and migration. Pre-treatment of mitogen-activated protein kinase kinase (MEK) inhibitors and a phosphatidylinositol 3 kinases (PI3K) inhibitor attenuated cell proliferation and migration. However, inhibition of the SOC channels failed to prevent EGF-mediated ERK 1/2 and Akt phosphorylation.Conclusions
Our results showed that STIM1, Orai1, ERK 1/2, and Akt are key determinants of EGF-mediated cell growth in ARPE-19 cells. EGF is a potent growth molecule that has been linked to the development of PVR, and therefore, STIM1, Orai1, as well as the MEK/ERK 1/2 and PI3K/Akt pathways, might be potential therapeutic targets for drugs aimed at treating such disorders. 相似文献7.
Rob J. Van Geest Ingeborg Klaassen Sarit Y. Lesnik-Oberstein H. Stevie Tan Marco Mura Roel Goldschmeding Cornelis J. F. Van Noorden Reinier O. Schlingemann 《Journal of cell communication and signaling》2013,7(1):1-9
In proliferative diabetic retinopathy (PDR), vascular endothelial growth factor (VEGF) and CCN2 (connective tissue growth factor; CTGF) cause blindness by neovascularization and subsequent fibrosis. This angio-fibrotic switch is associated with a shift in the balance between vitreous levels of CCN2 and VEGF in the eye. Here, we investigated the possible involvement of other important mediators of fibrosis, tissue inhibitor of metalloproteinases (TIMP)-1 and transforming growth factor (TGF)-β2, and of the matrix metalloproteinases (MMP)-2 and MMP-9, in the natural course of PDR. TIMP-1, activated TGF-β2, CCN2 and VEGF levels were measured by ELISA in 78 vitreous samples of patients with PDR (n = 28), diabetic patients without PDR (n = 24), and patients with the diabetes-unrelated retinal conditions macular hole (n = 10) or macular pucker (n = 16), and were related to MMP-2 and MMP-9 activity on zymograms and to clinical data, including degree of intra-ocular neovascularization and fibrosis. TIMP-1, CCN2 and VEGF levels, but not activated TGF-β2 levels, were significantly increased in the vitreous of diabetic patients, with the highest levels in PDR patients. CCN2 and the CCN2/VEGF ratio were the strongest predictors of degree of fibrosis. In diabetic patients with or without PDR, activated TGF-β2 levels correlated with TIMP-1 levels, whereas in PDR patients, TIMP-1 levels, MMP-2 and proMMP-9 were associated with degree of neovascularization, like VEGF levels, but not with fibrosis. We confirm here our previous findings that retinal fibrosis in PDR patients is significantly correlated with vitreous CCN2 levels and the CCN2/VEGF ratio. In contrast, TIMP-1, MMP-2 and MMP-9 appear to have a role in the angiogenic phase rather than in the fibrotic phase of PDR. 相似文献
8.
Susmitha Valli Gogula Ch Divakar Ch Satyanarayana Yedla Phani Kumar Vadapalli Santhosi Lavanaya 《Bioinformation》2013,9(20):1040-1043
Diabetic Retinopathy (DR) is one of the attenuating complications of diabetes mellitus. The key gene responsible for causing
diabetic retinopathy is protein kinase C beta (PKCβ). Protein kinase C is a family of protein kinase enzymes which are involved in
controlling the function of other proteins through phosphorylation mechanism and plays a crucial role in signal transduction
mechanisms. Among all the PKC isoenzymes, PKCβ could be a significant isoenzyme involved in vascular dysfunction during
hyperglycemia. Studies show that oral administration of PKCβ inhibitor Ruboxistaurin (), decreases vessel permeability
and improves retinal condition. Thus compounds that decrease the PKCβ activation would be helpful in the treatment of diabetic
retinopathy. The compounds similar to Ruboxistaurin are taken from Super Target database and docking analysis was performed.
Maleimide derivative 3 showed highest binding affinities compared to Ruboxistaurin and so we advise that compound may be
utilized in the treatment of diabetic retinopathy. LY333531相似文献
9.
Diagnosis and phylogenetic analysis of orf virus in Aleppo and Saanen goats from an outbreak in Turkey 总被引:1,自引:0,他引:1
正Dear Editor,The Poxviridae family is divided into Chordopoxvirinae and Entomopoxvirinae genera.Parapoxvirus is one of 11genera in the Chordopoxvirinae genus,including orf virus(ORFV),bovine papular stomatitis virus(BPSV),pseudocowpox virus(PCPV)and parapoxvirus of red deer in New Zealand(PVNZ)(Skinner et al.,2012).This virus,also known as contagious ecthyma or contagious pustular dermatitis,is a viral skin disease causing edematous proliferative lesions,most often in hairless skin 相似文献
10.
Maria Troullinaki Vasileia‐Ismini Alexaki Ioannis Mitroulis Anke Witt Anne Klotzschevon Ameln Kyoung‐Jin Chung Triantafyllos Chavakis Matina Economopoulou 《Journal of cellular and molecular medicine》2019,23(4):2362-2371
The mechanism underlying vasoproliferative retinopathies like retinopathy of prematurity (ROP) is hypoxia‐triggered neovascularisation. Nerve growth factor (NGF), a neurotrophin supporting survival and differentiation of neuronal cells may also regulate endothelial cell functions. Here we studied the role of NGF in pathological retinal angiogenesis in the course of the ROP mouse model. Topical application of NGF enhanced while intraocular injections of anti‐NGF neutralizing antibody reduced pathological retinal vascularization in mice subjected to the ROP model. The pro‐angiogenic effect of NGF in the retina was mediated by inhibition of retinal endothelial cell apoptosis. In vitro, NGF decreased the intrinsic (mitochondria‐dependent) apoptosis in hypoxia‐treated human retinal microvascular endothelial cells and preserved the mitochondrial membrane potential. The anti‐apoptotic effect of NGF was associated with increased BCL2 and reduced BAX, as well as with enhanced ERK and AKT phosphorylation, and was abolished by inhibition of the AKT pathway. Our findings reveal an anti‐apoptotic role of NGF in the hypoxic retinal endothelium, which is involved in promoting pathological retinal vascularization, thereby pointing to NGF as a potential target for proliferative retinopathies. 相似文献