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Cells
Special Issues
Mechanotransduction in Cellular Function and Diseases
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Mechanotransduction in Cellular Function and Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (5 June 2022) | Viewed by 2550

Special Issue Editor

Prof. Dr. Wan Lee

E-Mail Website
Guest Editor
1. Department of Biochemistry, Dongguk University School of Medicine, Gyeongju 38066, Republic of Korea
2. Channelopathy Research Center (CRC), Dongguk University School of Medicine, Ilsan 10326, Republic of Korea
Interests: mechanotransduction; cytoskeleton remodeling; proliferation; differentiation; myogenesis; sarcopenia; insulin resistance; diabetes; metabolism; glucose metabolism; lipid metabolism; metabolic diseases; energy metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mechanotransduction is the process by which a mechanical signal is converted into a series of biochemical transduction cascades, followed by cellular responses, referring to the capacity of cells to actively perceive, integrate, and turn into biochemical signals and responses. Although the molecular mechanisms underlying mechanotransduction remain unclear, over the last decade, growing evidence has suggested that it is crucial for various biological processes, including cell migration, proliferation, growth, differentiation, organ development, and tissue homeostasis. Therefore, the dysregulation of the transduction of mechanical cues into biochemical signals has been causally linked to the pathogenesis of many illnesses, such as cancer and degenerative and metabolic diseases.

This Special Issue includes all aspects of research focused on how mechanotransduction regulates cell signaling, cytoskeleton dynamics, apoptosis, proliferation, cell cycle, and differentiation. We welcome original research and reviews regarding all areas of mechanotransduction in health and illness.

Prof. Dr. Wan Lee
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mechanotransduction
  • mechanoreceptor
  • mechanoregulator
  • hippo signaling
  • YAP
  • TAZ
  • TEAD
  • proliferation
  • cancer
  • metabolic diseases

Published Papers (1 paper)

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Research

13 pages, 2035 KiB  
Article
Kank1 Is Essential for Myogenic Differentiation by Regulating Actin Remodeling and Cell Proliferation in C2C12 Progenitor Cells
by Mai Thi Nguyen and Wan Lee
Cells 2022, 11(13), 2030; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11132030 - 26 Jun 2022
Cited by 5 | Viewed by 1985
Abstract
Actin cytoskeleton dynamics are essential regulatory processes in muscle development, growth, and regeneration due to their modulation of mechanotransduction, cell proliferation, differentiation, and morphological changes. Although the KN motif and ankyrin repeat domain-containing protein 1 (Kank1) plays a significant role in cell adhesion [...] Read more.
Actin cytoskeleton dynamics are essential regulatory processes in muscle development, growth, and regeneration due to their modulation of mechanotransduction, cell proliferation, differentiation, and morphological changes. Although the KN motif and ankyrin repeat domain-containing protein 1 (Kank1) plays a significant role in cell adhesion dynamics, actin polymerization, and cell proliferation in various cells, the functional significance of Kank1 during the myogenic differentiation of progenitor cells has not been explored. Here, we report that Kank1 acts as a critical regulator of the proliferation and differentiation of muscle progenitor cells. Kank1 was found to be expressed at a relatively high level in C2C12 myoblasts, and its expression was modulated during the differentiation. Depletion of Kank1 by siRNA (siKank1) increased the accumulation of filamentous actin (F-actin). Furthermore, it facilitated the nuclear localization of Yes-associated protein 1 (YAP1) by diminishing YAP1 phosphorylation in the cytoplasm, which activated the transcriptions of YAP1 target genes and promoted proliferation and cell cycle progression in myoblasts. Notably, depletion of Kank1 suppressed the protein expression of myogenic regulatory factors (i.e., MyoD and MyoG) and dramatically inhibited myoblast differentiation and myotube formation. Our results show that Kank1 is an essential regulator of actin dynamics, YAP1 activation, and cell proliferation and that its depletion impairs the myogenic differentiation of progenitor cells by promoting myoblast proliferation triggered by the F-actin-induced nuclear translocation of YAP1. Full article
(This article belongs to the Special Issue Mechanotransduction in Cellular Function and Diseases)
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