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Diminished Integrin α3β1 Function in Epidermis Appears to Underlie Age-Related Healing Delays
Sanjana Dhulipalla
*2, Giesse Albeche Duarte
1, Palak Patel
1, Melissa S. Price
2, Rogger Andrade
1, Lei Wu
1, John Lamar
1, C. Michael DiPersio
1, Whitney Longmate
11Molecular and Cellular Physiology, Albany Medical College, Albany, NY; 2Division of Plastic Surgery, Albany Medical Center, Albany, NY
Background: Wound re-epithelialization is essential for skin repair but declines with age, placing significant burden on elderly patients and the healthcare system. Epidermal integrin α3β1 has been implicated in keratinocyte proliferation and migration, both critical for efficient healing. Using a novel epidermis-specific, inducible knockout model (iα3eKO), we previously identified α3β1's role in promoting wound closure in young mice. Since healing is delayed with age, we investigated whether α3β1 function is impaired in aged skin and whether this impairment underlies age-related healing delays.
Methods: Young (2-month-old) and aged (22-month-old) control and iα3eKO mice were wounded by 4mm biopsy punch. Frozen sections were immunostained for α3, K14, Ki67, and DAPI. α3β1 expression, keratinocyte proliferation, and re-epithelialization were compared across age groups. Human skin samples from surgical patients were analyzed under IRB approval to assess age-related α3β1 expression.
Results: In young mice, α3β1 deletion reduced re-epithelialization (p<0.0001) and keratinocyte proliferation in wound-distal follicles (p=0.0235). Resting epidermal α3 expression was similar between age groups; however, aged mice fail to upregulate α3β1 after wounding. Aged controls displayed delayed closure and reduced proliferation compared to young controls, and α3β1 deletion conferred no further impairment in aged mice. Bioinformatics revealed decreased β1 expression with age in human skin datasets and our preliminary work in human skin are consistent with impaired α3β1 expression with age.
Conclusions: Epidermal α3β1 function is impaired in aged wounds, contributing to reduced keratinocyte proliferation and delayed re-epithelialization. These findings highlight α3β1 as a promising therapeutic target to enhance wound healing in elderly patients.
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