Abstract:
:MiR-204 is expressed in vascular smooth muscle cells (VSMC). However, its role in VSMC contraction is not known. We determined if miR-204 controls VSMC contractility and blood pressure through regulation of sarcoplasmic reticulum (SR) calcium (Ca2+) release. Systolic blood pressure (SBP) and vasoreactivity to VSMC contractile agonists (phenylephrine (PE), thromboxane analogue (U46619), endothelin-1 (ET-1), angiotensin-II (Ang II) and norepinephrine (NE) were compared in aortas and mesenteric resistance arteries (MRA) from miR-204-/- mice and wildtype mice (WT). There was no difference in basal systolic blood pressure (SBP) between the two genotypes; however, hypertensive response to Ang II was significantly greater in miR-204-/- mice compared to WT mice. Aortas and MRA of miR-204-/- mice had heightened contractility to all VSMC agonists. In silico algorithms predicted the type 1 Inositol 1, 4, 5-trisphosphate receptor (IP3R1) as a target of miR-204. Aortas and MRA of miR-204-/- mice had higher expression of IP3R1 compared to WT mice. Difference in agonist-induced vasoconstriction between miR-204-/- and WT mice was abolished with pharmacologic inhibition of IP3R1. Furthermore, Ang II-induced aortic IP3R1 was greater in miR-204-/- mice compared to WT mice. In addition, difference in aortic vasoconstriction to VSMC agonists between miR-204-/- and WT mice persisted after Ang II infusion. Inhibition of miR-204 in VSMC in vitro increased IP3R1, and boosted SR Ca2+ release in response to PE, while overexpression of miR-204 downregulated IP3R1. Finally, a sequence-specific nucleotide blocker that targets the miR-204-IP3R1 interaction rescued miR-204-induced downregulation of IP3R1. We conclude that miR-204 controls VSMC contractility and blood pressure through IP3R1-dependent regulation of SR calcium release.
journal_name
Cell Calciumjournal_title
Cell calciumauthors
Gabani M,Liu J,Ait-Aissa K,Koval O,Kim YR,Castañeda D,Vikram A,Jacobs JS,Grumbach I,Trebak M,Irani K,Kassan Mdoi
10.1016/j.ceca.2019.03.006subject
Has Abstractpub_date
2019-06-01 00:00:00pages
18-24eissn
0143-4160issn
1532-1991pii
S0143-4160(19)30033-8journal_volume
80pub_type
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