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Knockout of Angiotensin AT2 receptors accelerates healing but impairs quality
Mahya Faghih1, Sayed M Hosseini2, Barbara Smith3
1Division of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.
Abstract:
Wounds are among the most common, painful, debilitating and costly conditions in older adults. Disruption of the angiotensin type 1 receptors (AT1R), has been associated with impaired wound healing, suggesting a critical role for AT1R in this repair process. Biological functions of angiotensin type 2 receptors (AT2R) are less studied. We investigated effects of genetically disrupting AT2R on rate and quality of wound healing. Our results suggest that AT2R effects on rate of wound closure depends on the phase of wound healing. We observed delayed healing during early phase of wound healing (inflammation). An accelerated healing rate was seen during later stages (proliferation and remodeling). By day 12, fifty percent of AT2R(-/-) mice had complete wound closure as compared to none in either C57/BL6 or AT1R(-/-) mice. There was a significant increase in AT1R, TGFβ1 and TGFβ2 expression during the proliferative and remodeling phases in AT2R(-/-) mice. Despite the accelerated closure rate, AT2R(-/-) mice had more fragile healed skin. Our results suggest that in the absence of AT2R, wound healing rate is accelerated, but yielded worse skin quality. Elucidating the contribution of both of the angiotensin receptors may help fine tune future intervention aimed at wound repair in older individuals.
Insights
Disrupting angiotensin type 2 receptors (AT2R) accelerates wound healing rate but impairs skin quality. This suggests AT2R plays a complex role in the wound repair process, impacting both speed and integrity.
Area of Science:
- Biomedical Science
- Dermatology
- Wound Healing Research
Background:
- Wound healing is critical in older adults, with angiotensin type 1 receptors (AT1R) implicated in impaired repair.
- The biological functions of angiotensin type 2 receptors (AT2R) in wound healing remain less understood.
Purpose of the Study:
- To investigate the effects of genetically disrupting AT2R on the rate and quality of wound healing.
- To elucidate the role of AT2R in different phases of the wound repair process.
Main Methods:
- Utilized genetically modified mice lacking AT2R (AT2R-/-) for wound healing studies.
- Compared wound closure rates and skin quality in AT2R-/- mice against control groups (C57/BL6 and AT1R-/- mice).
- Analyzed the expression of AT1R, TGFβ1, and TGFβ2 during wound healing phases.
Main Results:
- AT2R disruption led to delayed healing during the early inflammatory phase but accelerated healing in later proliferation and remodeling stages.
- Fifty percent of AT2R-/- mice achieved complete wound closure by day 12, unlike control groups.
- Increased expression of AT1R, TGFβ1, and TGFβ2 was observed in AT2R-/- mice during proliferative and remodeling phases.
- Despite faster closure, AT2R-/- mice exhibited more fragile healed skin.
Conclusions:
- Absence of AT2R accelerates wound healing rate but compromises the quality and integrity of the healed skin.
- AT2R influences wound healing rate differentially across healing phases.
- Understanding the roles of both AT1R and AT2R is crucial for developing targeted interventions for wound repair, particularly in the elderly.
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