View : 15 Download: 0
Phospholipase C-β3 is dispensable for vascular constriction but indispensable for vascular hyperplasia
- Title
- Phospholipase C-β3 is dispensable for vascular constriction but indispensable for vascular hyperplasia
- Authors
- Jin; Seo Yeon; Ha; Jung Min; Kum; Hye Jin; Ma; Ji Soo; Hong Koo; Song; Sang Heon; Yang; Yong Ryoul; Lee; Ho; Bae; Yoon Soo; Yamamoto; Masahiro; Suh; Pann-Ghill; Sun Sik
- Ewha Authors
- 배윤수
- SCOPUS Author ID
- 배윤수
![scopus](/images/layout/icon2.png)
- Issue Date
- 2024
- Journal Title
- Experimental and Molecular Medicine
- ISSN
- 1226-3613
- Citation
- Experimental and Molecular Medicine vol. 56, no. 7, pp. 1620 - 1630
- Indexed
- SCIE; SCOPUS; KCI
![scopus](/images/layout/scopus2.gif)
- Document Type
- Article
- Abstract
- Angiotensin II (AngII) induces the contraction and proliferation of vascular smooth muscle cells (VSMCs). AngII activates phospholipase C-β (PLC-β), thereby inducing Ca2+ mobilization as well as the production of reactive oxygen species (ROS). Since contraction is a unique property of contractile VSMCs, signaling cascades related to the proliferation of VSMCs may differ. However, the specific molecular mechanism that controls the contraction or proliferation of VSMCs remains unclear. AngII-induced ROS production, migration, and proliferation were suppressed by inhibiting PLC-β3, inositol trisphosphate (IP3) receptor, and NOX or by silencing PLC-β3 or NOX1 but not by NOX4. However, pharmacological inhibition or silencing of PLC-β3 or NOX did not affect AngII-induced VSMC contraction. Furthermore, the AngII-dependent constriction of mesenteric arteries isolated from PLC-β3∆SMC, NOX1−/−, NOX4−/− and normal control mice was similar. AngII-induced VSMC contraction and mesenteric artery constriction were blocked by inhibiting the L-type calcium channel Rho-associated kinase 2 (ROCK2) or myosin light chain kinase (MLCK). The activation of ROCK2 and MLCK was significantly induced in PLC-β3∆SMC mice, whereas the depletion of Ca2+ in the extracellular medium suppressed the AngII-induced activation of ROCK2, MLCK, and vasoconstriction. AngII-induced hypertension was significantly induced in NOX1−/− and PLC-β3∆SMC mice, whereas LCCA ligation-induced neointima formation was significantly suppressed in NOX1−/− and PLC-β3∆SMC mice. These results suggest that PLC-β3 is essential for vascular hyperplasia through NOX1-mediated ROS production but is nonessential for vascular constriction or blood pressure regulation. © The Author(s) 2024.
- DOI
- 10.1038/s12276-024-01271-6
- Appears in Collections:
- 자연과학대학 > 생명과학전공 > Journal papers
- Files in This Item:
There are no files associated with this item.
- Export
- RIS (EndNote)
- XLS (Excel)
- XML