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991.
David S. Gokhin Roberta B. Nowak Nancy E. Kim Ernest E. Arnett Albert C. Chen Robert L. Sah John I. Clark Velia M. Fowler 《PloS one》2012,7(11)
The basis for mammalian lens fiber cell organization, transparency, and biomechanical properties has contributions from two specialized cytoskeletal systems: the spectrin-actin membrane skeleton and beaded filament cytoskeleton. The spectrin-actin membrane skeleton predominantly consists of α2β2-spectrin strands interconnecting short, tropomyosin-coated actin filaments, which are stabilized by pointed-end capping by tropomodulin 1 (Tmod1) and structurally disrupted in the absence of Tmod1. The beaded filament cytoskeleton consists of the intermediate filament proteins CP49 and filensin, which require CP49 for assembly and contribute to lens transparency and biomechanics. To assess the simultaneous physiological contributions of these cytoskeletal networks and uncover potential functional synergy between them, we subjected lenses from mice lacking Tmod1, CP49, or both to a battery of structural and physiological assays to analyze fiber cell disorder, light scattering, and compressive biomechanical properties. Findings show that deletion of Tmod1 and/or CP49 increases lens fiber cell disorder and light scattering while impairing compressive load-bearing, with the double mutant exhibiting a distinct phenotype compared to either single mutant. Moreover, Tmod1 is in a protein complex with CP49 and filensin, indicating that the spectrin-actin network and beaded filament cytoskeleton are biochemically linked. These experiments reveal that the spectrin-actin membrane skeleton and beaded filament cytoskeleton establish a novel functional synergy critical for regulating lens fiber cell geometry, transparency, and mechanical stiffness. 相似文献
992.
Bruce L. Riser Feridoon Najmabadi Bernard Perbal Jo Ann Rambow Melisa L. Riser Ernest Sukowski Herman Yeger Sarah C. Riser Darryl R. Peterson 《Journal of cell communication and signaling》2010,4(1):39-50
Prior work in the CCN field, including our own, suggested to us that there might be co-regulatory activity and function as
part of the actions of this family of cysteine rich cytokines. CCN2 is now regarded as a major pro-fibrotic molecule acting
both down-stream and independent of TGF-β1, and appears causal in the disease afflicting multiple organs. Since diabetic renal
fibrosis is a common complication of diabetes, and a major cause of end stage renal disease (ESRD), we examined the possibility
that CCN3 (NOV), might act as an endogenous negative regulator of CCN2 with the capacity to limit the overproduction of extracellular
matrix (ECM), and thus prevent, or ameliorate fibrosis. We demonstrate, using an in vitro model of diabetic renal fibrosis,
that both exogenous treatment with CCN3 and transfection with the over-expression of the CCN3 gene in mesangial cells markedly
down-regulates CCN2 activity and blocks ECM over-accumulation stimulated by TGF-β1. Conversely, TGF-β1 treatment reduces endogenous
CCN3 expression and increases CCN2 activity and matrix accumulation, indicating an important, novel yin/yang effect. Using
the db/db mouse model of diabetic nephropathy, we confirm the expression of CCN3 in the kidney, with temporal localization
that supports these in vitro findings. In summary, the results corroborate our hypothesis that one function of CCN3 is to
regulate CCN2 activity and at the concentrations and conditions used down-regulates the effects of TGF-β1, acting to limit
ECM turnover and fibrosis in vivo. The findings suggest opportunities for novel endogenous-based therapy either by the administration,
or the upregulation of CCN3. 相似文献
993.
Structural basis of contraction in vertebrate smooth muscle 总被引:9,自引:0,他引:9
994.
Inhibition of cell expansion of excised embryonic axes of Phaseolus vulgaris was used to evaluate the growth-inhibiting activity of abscisic acid and related compounds. None of the 13 compounds tested was as active as abscisic acid. 4-Hydroxyisophorone, a substance representative of the abscisic acid ring system was essentially inactive; cis, trans-3-methylsorbic acid, a compound resembling the side chain of abscisic acid, had low activity; and cis, trans-beta-ionylideneacetic acid was one-sixth as active. Loss of the ring double bond results in a drastic decrease in biological activity. Comparison of our results with those reported previously leads to the suggestion that the double bond of the cyclohexyl moiety may have an important function in determining the degree of activity of cis, trans-ionylideneacetic acids. Two modes of action are discussed. It seems possible that the ring double bond is involved in covalent bonding in binding of the abscisic acid analogue to macromolecules. This may require formation of an intermediate epoxide. It can also be argued that stereochemical differences between cyclohexane derivatives are important factors in determining the degree of biological activity. 相似文献
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