Expression of Protein Kinases RIPK-1 and RIPK-3 in Mouse and Human Hair Follicle
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HEMISTRY, BIOPHYSICS, AND MOLECULAR BIOLOGY
Expression of Protein Kinases RIPK-1 and RIPK-3 in Mouse and Human Hair Follicle E. I. Morguna,b,*, E. D. Pozdniakovac, and Corresponding Member of the RAS E. A. Vorotelyakb Received May 19, 2020; revised May 22, 2020; accepted May 25, 2020
Abstract— Expression of cell death regulators RIPK-1 and RIPK-3 in mouse and human hair follicle structures was studied by immunohistochemistry. At anagen and catagen stages of mouse hair follicle, RIPK-1+ cells were located in the inner root sheath, whereas RIPK-3+ cells were found in the inner and outer root sheath, dermal papilla, and interfollicular epidermis. RIPK-1 expression intensity was low in the early anagen and increased as mature anagen and catagen approached. RIPK-1+ and RIPK-3+ cells were also found in human hair follicle. It is assumed that the role of necroptosis markers in hair follicle life activity is independent of programmed cell death and that they may have yet unknown functions and take part in noncanonical signal cascades. Keywords: hair follicle, necroptosis, RIPK-1, RIPK-3, programmed cell death, anagen, catagen DOI: 10.1134/S1607672920050105
The hair follicle (HF) is a mammalian mini-organ whose structure undergoes cyclic changes throughout life. In the telogen phase, the HF is in a state of metabolic rest in the form of a small group of cells, in the growth phase (anagen) its keratinocytes proliferate and differentiate to form a normal HF, and in catagen the HF structure undergoes partial regression. Programmed cell death is an essential part of the normal life of the HF. For example, the hair follicle undergoes involution in catagen via apoptosis of keratinocytes [1], and the hair shaft is formed due to a special type of cell death, keratinization, which the cells of the inner root sheath undergo [2]. However, the mechanisms of these processes are still not fully understood: not all components of signaling pathways of apoptosis [3] and keratinization [2], as well as their intersection points, have been studied. For this reason, we studied HF for the expression of markers of another type of programmed cell death, necroptosis, in which RIPK-1 (receptor-interacting protein kinase-1) and RIPK-3 (receptor-interacting protein kinase-3) are involved [4]. In an inactive state, RIPK-1 as a component of multicomponent protein complexes can promote cell survival. As a result of, for example, inhibition of IKKα/β- and TBK1/IKKε-dependent phosphorylaa Moscow
Institute of Physics and Technology (State University), Dolgoprudny, Moscow, Russia b Koltzov Institute of Developmental Biology, Russian Academy of Sciences, Moscow, Russia c Moscow State University, Moscow, Russia *e-mail: [email protected]
tion, the realization of the kinase activity of RIPK-1 becomes possible, which leads to cell death [5]. The activity of RIPK-3 depends on RIPK-1; however, there is no evidence that RIPK-1 phosphorylates RIPK-3. Probably, RIPK-1 and RIPK-3 are activated by autophosphorylation; however, this process has not been studi
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