Angiogenesis Related Roles of Induced Pluripotent Stem Cells in Wound Healing


Ocak H., Özen A.

7th International Conference on Advances in Natural and Applied Sciences (ICANAS 2024) , Antalya, Türkiye, 17 - 20 Nisan 2024, ss.147-148, (Özet Bildiri)

  • Yayın Türü: Bildiri / Özet Bildiri
  • Basıldığı Şehir: Antalya
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.147-148
  • Ankara Üniversitesi Adresli: Evet

Özet

Wound healing is a type of regeneration involving 4 consecutive stages: haemostasis,

inflammation, proliferation and remodeling. Occuring mainly in proliferative phase

vasculature formation is a vital step for wound healing. Induced pluripotent stem cells

(iPSCs) have invaluable capacity for tissue regeneration and wound healing because of

their ability to differentiate into multiple cell lineages, lack of immune rejection and

ethical concerns.

Studies in the literature could be divided to 4 groups: cellular differentiation based,

exosome based, scaffold-biomaterials based and gene based studies. First group of

studies involve differentiation of iPSCs to smooth muscle cells (SMCs), epithelial cells

(ECs), keratinocytes. Mainly these iPSCs derived SMCs enhanced wound healing via

angiogenesis by increasing growth factors and cytokines such as bFGF, VEGF (1, 2),

cellular proliferation, survival of hiPSCs and macrophage polarization (2), collagen

deposition, macrophage infiltration (3), increased blood vessel density and growth

factors (4).

iPSCs derived exosomes-microvesicles improved wound healing by improved collagen I

and III levels, reduced inflammation (5), thickening epidermis and increased collagen

deposition and α-smooth muscle actin (α-SMA) together with CD31 (6), increased

number of nerve fibers and α-SMA and CD31 (7). In another study they increased wound

healing by improved collagen-elastin deposition and vessel density (8).

Collagen scaffolds with hIPSCs derived SMCs healed wound by epidermal and dermal

thickening, enhanced cytokines and growth factors (9). Human skin substitute with

fibroblasts and keratinocytes improved wound healing by neovascularization, and blood

vessel invasion from wound bed (10).

When integrin β1 was knocked out in iPSCs, it resulted with improved iPSCs migration

and survival, angiogenesis, blood perfusion and consequently wound healing (11).