The cellular origin of laminin determines its role in blood pressure regulation.
The cellular origin of laminin determines its role in blood pressure regulation.
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DOI：
10.1007/s00018-014-1732-y
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发表时间：
2015-03
影响因子：
8
通讯作者：
Strickland, Sidney
中科院分区：
文献类型：
--
作者：
Yao, Yao;Norris, Erin H.;Strickland, Sidney
不同细胞来源的层粘连蛋白具有不同的功能。除了血管平滑肌细胞（SMC），主动脉还含有少量巢蛋白+细胞，其功能尚不清楚。本研究探讨了SMC和巢蛋白+细胞源性层粘连蛋白在血压（BP）调节和SMC收缩性中的作用。使用SMC（SKO）或nestin+细胞（NKO）层粘连蛋白缺乏的小鼠，我们检查了基线BP的层粘连蛋白依赖性变化。收缩蛋白表达在SKO而非NKO小鼠中减少，与它们分别低和正常的基线BP测量结果一致。在超微结构水平上，SKO SMC保持收缩表型，弹性降低，而NKO SMC转换为合成表型并显示变性。此外，血管紧张素II（Ang II）显着增加血压在SKO但不是NKO小鼠。它还将两种基因敲除小鼠的收缩蛋白提高到相同水平，并诱导SMC变性。这些数据表明，SMC层粘连蛋白通过调节收缩蛋白的表达来调节血压，而巢蛋白+细胞源性层粘连蛋白有助于SMC表型转换。
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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影响因子：
37.8
作者：
Roger VL;Go AS;Lloyd-Jones DM;Benjamin EJ;Berry JD;Borden WB;Bravata DM;Dai S;Ford ES;Fox CS;Fullerton HJ;Gillespie C;Hailpern SM;Heit JA;Howard VJ;Kissela BM;Kittner SJ;Lackland DT;Lichtman JH;Lisabeth LD;Makuc DM;Marcus GM;Marelli A;Matchar DB;Moy CS;Mozaffarian D;Mussolino ME;Nichol G;Paynter NP;Soliman EZ;Sorlie PD;Sotoodehnia N;Turan TN;Virani SS;Wong ND;Woo D;Turner MB;American Heart Association Statistics Committee and Stroke Statistics Subcommittee
通讯作者：
American Heart Association Statistics Committee and Stroke Statistics Subcommittee
DOI：
10.1083/jcb.201212032
发表时间：
2013-07-22
期刊：
The Journal of cell biology
影响因子：
--
作者：
Chen ZL;Yao Y;Norris EH;Kruyer A;Jno-Charles O;Akhmerov A;Strickland S
通讯作者：
Strickland S
影响因子：
5
作者：
Hassane, Sabrine;Claij, Nanna;Peters, Dorien J. M.
通讯作者：
Peters, Dorien J. M.
影响因子：
0.9
作者：
Kochova, Petra;Tonar, Zbynek;Kuncova, Jitka
通讯作者：
Kuncova, Jitka
影响因子：
1.5
作者：
Dubois, Nicole C.;Hofmann, Denise;Trumpp, Andreas
通讯作者：
Trumpp, Andreas