Abstract
Primary cilia (PC) are solitary, post-mitotic, microtubule-based, and membrane-covered protrusions that are found on almost every mammalian cell. PC are specialized cellular sensory organelles that transmit environmental information to the cell. Signaling through PC is involved in the regulation of a variety of cellular processes, including proliferation, differentiation, and migration. Conversely, defective, or abnormal PC signaling can contribute to the development of various pathological conditions. Our knowledge of the role of PC in organ development and function is largely based on ciliopathies, a family of genetic disorders with mutations affecting the structure and function of PC. In this review, we focus on the role of PC in their major signaling pathways active in skin cells, and their contribution to wound healing and scarring. To provide comprehensive insights into the current understanding of PC functions, we have collected data available in the literature, including evidence across cell types, tissues, and animal species. We conclude that PC are underappreciated subcellular organelles that significantly contribute to both physiological and pathological processes of the skin development and wound healing. Thus, PC assembly and disassembly and PC signaling may serve as attractive targets for antifibrotic and antiscarring therapies.
Highlights
The wound healing cascade progresses through the partially overlapping stages of hemostasis, inflammation, repair/proliferation, and remodeling (Almine et al, 2012)
The aim of this review is to summarize the current understanding of primary cilia (PC) functions and their main signaling pathways associated with inflammation, scar formation, and wound healing under normal and pathological conditions
Since these signaling pathways are governed by Primary cilia (PC), these results further suggest a central role of signaling through preadipocyte and fibroblast PC in the control of wound healing
Summary
The wound healing cascade progresses through the partially overlapping stages of hemostasis, inflammation, repair/proliferation, and remodeling (Almine et al, 2012). Granulation tissue cells produce TGF-β 1 and TGF-β 2, which in turn induce fibroblasts to proliferate and synthesize the provisional ECM. Upon the transition from granulation tissue to a scar, in the remodeling phase, the abundant type III collagen that dominates the proliferation stage ECM is largely replaced by type I collagen through the balanced activity of matrix metalloproteinases and their tissue inhibitors (Singer and Clark, 1999). This leads to the formation of a relatively acellular scar. We collected literature across species, cell, and tissue types as well as disease models to provide further insight into the possible roles of the PC in skin
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