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10.1007/s00018-014-1732-y

http://scihub22266oqcxt.onion/10.1007/s00018-014-1732-y
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C4323860!4323860!25216704
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suck abstract from ncbi


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pmid25216704      Cell+Mol+Life+Sci 2015 ; 72 (5): 999-1008
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  • The cellular origin of laminin determines its role in blood pressure regulation #MMPMID25216704
  • Yao Y; Norris EH; Strickland S
  • Cell Mol Life Sci 2015[Mar]; 72 (5): 999-1008 PMID25216704show ga
  • Laminin of different cellular source has distinct functions. In addition to vascular smooth muscle cells (SMCs), aorta also contains a small population of nestin+ cells, whose function remains unknown. This study investigates the role of SMC- and nestin+ cell-derived laminin in blood pressure (BP) regulation and SMC contractibility. Using mice with laminin deficiency in SMCs (SKO) or nestin+ cells (NKO), we examined laminin-dependent changes in baseline BP. Contractile protein expression was reduced in SKO but not NKO mice, consistent with their respectively low and normal baseline BP measurements. At the ultrastructural level, SKO SMCs maintained the contractile phenotype with reduced elasticity, whereas NKO SMCs switched to the synthetic phenotype and showed degeneration. Additionally, angiotensin II (Ang II) significantly increased BP in SKO but not NKO mice. It also enhanced contractile proteins to the same levels and induced SMC degeneration in both knockout mice. These data suggest that SMC laminin regulates BP via modulating contractile protein expression, whereas nestin+ cell-derived laminin contributes to SMC phenotypic switch.
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