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Updated: Sep 27, 2026
Isolation of Retinal Arterioles for Ex Vivo Cell Physiology Studies
Published on: July 14, 2018
Failure of angiotensin II and insulin to stimulate transforming growth factor-beta1. Release from cultured bovine
P Limone1, C Berardi, F Pomero
1Department of Internal Medicine, University of Torino, Italy. paolopiero.limone@unito.it
Background:
Activation of the renin-angiotensin system (RAS) may induce cardiovascular and renal fibrosis in hypertension and diabetes. This fibrogenic effect is mainly mediated by Transforming Growth Factor-B1 (TGF-B1), a multifunctional citokyne released by endothelial, vascular smooth muscle and renal mesangial cells, that is able to increase extracellular matrix deposition. Retinal capillary pericytes have functions similar to those of mesangial cells, including ability to synthesize and release TGF-B1 and produce extracellular matrix. An intraocular RAS was described in the human eye and may produce effects similar to those observed in the heart and kidney, which could be mediated by TGF-B1. In particular, TGF-B1 might be involved in thickening of the capillary basement membrane in diabetic microangiopathy. We therefore aimed at evaluating the possible effects of Angiotensin-II on TGF-B1 secretion by cultured retinal pericytes (BRP).
Methods:
BRP cultures were incubated with Angiotensin-II or insulin (known to play a permissive effect on TGF-B1 release from mesangial cells) or Angiotensin-II + insulin at final concentrations of 10-10, 10-8, 10-6, 10-4 mol/L.
Results:
Baseline TGF-B1 concentrations in the supernatants of pericyte cultures were 6 139 +/- 1 919 pg/mL/106 cells; no changes of TGF-B1 concentrations resulted from adding increasing amounts of Ang II, insulin or both.
Conclusions:
Though confirming that cultured bovine retinal pericytes spontaneously release TGF-B1, Angiotensin-II did not produce any stimulatory effects of in our experimental system
Insights
Angiotensin-II does not stimulate Transforming Growth Factor-B1 (TGF-B1) release from bovine retinal pericytes. This suggests Angiotensin-II may not directly contribute to fibrosis in the eye via TGF-B1 in this experimental model.
Area of Science:
- Ophthalmology
- Cardiovascular Research
- Endocrinology
Background:
- The renin-angiotensin system (RAS) contributes to cardiovascular and renal fibrosis, primarily through Transforming Growth Factor-B1 (TGF-B1).
- Retinal pericytes share functional similarities with mesangial cells, including TGF-B1 synthesis and extracellular matrix production.
- An intraocular RAS may influence ocular conditions like diabetic microangiopathy, potentially involving TGF-B1 and basement membrane thickening.
Purpose of the Study:
- To investigate the effect of Angiotensin-II on TGF-B1 secretion by cultured bovine retinal pericytes (BRP).
- To explore the potential role of Angiotensin-II in mediating fibrotic processes within the retinal microvasculature.
Main Methods:
- Cultured BRP were treated with varying concentrations of Angiotensin-II, insulin, or a combination of both.
- TGF-B1 concentrations in the cell culture supernatant were measured.
Main Results:
- Bovine retinal pericytes exhibited spontaneous release of TGF-B1.
- Neither Angiotensin-II, insulin, nor their combination significantly altered TGF-B1 concentrations in the pericyte cultures.
Conclusions:
- Cultured bovine retinal pericytes spontaneously secrete TGF-B1.
- Angiotensin-II did not demonstrate a stimulatory effect on TGF-B1 secretion in this experimental system.
- These findings suggest Angiotensin-II may not directly induce TGF-B1-mediated fibrosis in retinal pericytes.
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