Akt/eNOS and MAPK signaling pathways mediated the phenotypic switching of thoracic aorta vascular smooth muscle cells in aging/hypertensive rats.

Abstract:

:Considerable evidence demonstrates that phenotypic switching of vascular smooth muscle cells (VSMCs) is influenced by aging and hypertension. During phenotypic switching, VSMCs undergo a switch to a proliferative and migratory phenotype, with this switch being a common pathology in cardiovascular diseases. The aim of this study was to explore the joint influence of age and hypertension on thoracic aortic smooth muscle phenotypic switching and the balance of Akt and mitogen-activated protein kinase (MAPK) signaling during this switch. Different ages of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were used to establish hypertension and aging models. The phenotypic state was determined by detecting the marker proteins alpha-SM-actin, calponin, and osteopontin (OPN) via immunohistochemical staining and Western blot. Signaling proteins associated with the Akt and MAPK pathways were detected in rat thoracic aorta using Western blot. Both aging and hypertension caused a decrease in contractile (differentiated) phenotype markers (alpha-SM-actin and calponin), while the synthetic (proliferative or de-differentiated) phenotype maker was elevated (OPN). When combining hypertension and aging, this effect was enhanced, with Akt signaling decreased, while MAPK signaling was increased. These results suggested that VSMCs phenotype switching is modulated by a balance between Akt and MAPK signaling in the process of aging and hypertension.

journal_name

Physiol Res

journal_title

Physiological research

authors

Zhang L,Xu Z,Wu Y,Liao J,Zeng F,Shi L

doi

10.33549/physiolres.933779

subject

Has Abstract

pub_date

2018-08-16 00:00:00

pages

543-553

issue

4

eissn

0862-8408

issn

1802-9973

pii

933779

journal_volume

67

pub_type

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