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Published on: May 19, 2020
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IGF-1 receptor cleavage in hypertension
Selma Cirrik1, Geert W Schmid-Schönbein2
1Department of Physiology, Faculty of Medicine, Ordu University, Ordu, Turkey. selmacrrk@yahoo.com.
Summary
Hypertension increases protease activity, leading to insulin-like growth factor-1 receptor (IGF-1R) cleavage and reduced IGF-1 response. Matrix metalloproteinase (MMP) inhibition prevented this cleavage in spontaneously hypertensive rats.
Area of Science:
- Cardiovascular Biology
- Protease Biochemistry
- Endocrinology
Background:
- Hypertension is linked to impaired insulin-like growth factor-1 (IGF-1) signaling.
- Increased protease activity in hypertension can cause extracellular receptor cleavage, leading to dysfunction.
Purpose of the Study:
- To investigate the association between enhanced protease activity and IGF-1 receptor (IGF-1R) cleavage in spontaneously hypertensive rats (SHRs).
- To determine the impact of matrix metalloproteinase (MMP) activity on IGF-1R function in the aorta.
Main Methods:
- Compared MMP activity in plasma and tissues of SHRs and Wistar Kyoto (WKY) rats using gelatin zymography.
- Incubated WKY aorta rings with SHR plasma, with and without MMP inhibitors, assessing IGF-1R subunit density via immunohistochemistry.
- Analyzed downstream signaling (pAkt, peNOS) using immunoblotting to evaluate IGF-1R function.
Main Results:
- SHRs exhibited increased plasma and tissue MMP-2 and MMP-9 activity.
- SHR plasma reduced IGF-1R alpha subunit density in WKY aorta endothelium, an effect prevented by MMP inhibitors.
- SHRs showed lower pAkt and peNOS levels, indicating impaired IGF-1 signaling in the aorta.
Conclusions:
- Elevated MMP activity in hypertension contributes to IGF-1R alpha subunit cleavage.
- MMP-dependent IGF-1R cleavage impairs IGF-1 cellular response in the aorta of spontaneously hypertensive rats.
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