Development of angiotensin (1‐7) as an agent to accelerate dermal repair

Abstract

Angiotensin II has been shown to be a potent agent in the acceleration of wound repair. Angiotensin (1-7), a fragment of angiotensin II that is not hypertensive, was found to be comparable to angiotensin II in accelerating dermal healing. This activity was evaluated in four models: rat and diabetic mouse full-thickness excisional wounds; rat random flap; and guinea pig partial thickness thermal injury. In all models, angiotensin (1-7) was comparable to angiotensin II. Angiotensin (1-7) accelerated the closure of wounds in diabetic mice and rats. In diabetic mice the resultant tissue at day 25 after injury was more comparable to normal tissue than the fibrotic scar observed in placebo-treated wounds. In the random flap model, angiotensin (1-7) was comparable to angiotensin II in maintaining flap viability (approximately 82%) and flap survival (40%). Finally, angiotensin (1-7) increased proliferation in the hair follicles at the edge of the wound and site of thermal injury, and the number of patent blood vessels on day 7 after partial thickness thermal injury. These data may be partially explained by the effect of angiotensin II and angiotensin (1-7) on keratinocyte proliferation. While platelet-derived growth factor had no effect on keratinocyte proliferation, angiotensin II and angiotensin (1-7) significantly increased keratinocyte proliferation. These data show that angiotensin(1-7) is comparable to angiotensin II in accelerating skin repair. Furthermore, the hypertensive and wound healing effects can be separated within the family of angiotensin peptides.

Angiotensin-II Mediates Nonmuscle Myosin II Activation and Expression and Contributes to Human Keloid Disease Progression

“…Previous studies have demonstrated the role of Ang II in many aspects of wound repair (38). Exogenous administration of up to 100 μg Ang II per day improved diabetic wound healing in mice, and the Ang II analog (1-7) also improved wound healing (23,24).…”

Characterization and significance of ACE2 and Mas receptor in human colon adenocarcinoma

“…For instance, although Ang1-7 decreased the proliferation in several cell types, it also promoted cellular proliferation in the hair follicles at the edge of the wound and hematopoietic progenitors. 20,21 In addition, as for AngII, further studies on other human colon adenocarcinoma cell lines should be performed to fully evaluate the effect of Ang1-7 on cell cycle events in colon adenocarcinoma. Anyway, to link our data to the current literature, even though MasR is highly expressed in colon adenocarcinoma, it does not seem to be involved in any oncogenic pathway leading to cancer development.…”

Angiotensin II promotes melanogenesis via angiotensin II type 1 receptors in human melanocytes

“…Previous studies have demonstrated that angiotensin II (AngII) may be involved in all stages of wound healing (3), including inflammatory cell invasion, cell proliferation, cell migration, neovascularization and fibrosis (4). AngII has been observed to increase vascular permeability, recruit inflammatory cells (5,6), and promote keratinocyte proliferation (4,7,8) and dermal wound closure (9).…”

“…AngII has been observed to increase vascular permeability, recruit inflammatory cells (5,6), and promote keratinocyte proliferation (4,7,8) and dermal wound closure (9).…”