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Life
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Gene Regulation by HIFs under Hypoxia
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Gene Regulation by HIFs under Hypoxia

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Cell Biology and Tissue Engineering".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 2785

Special Issue Editor

Dr. Arvydas Kanopka

E-Mail Website
Guest Editor
Department of Immunology and Cell Biology, Institute of Biotechnology, Life Sciences Center, Vilnius University, 10257 Vilnius, Lithuania
Interests: cellular hypoxia; cancer biology; alternative splicing; RNA splicing; hypoxia dependent changes in cells; splicing factors

Special Issue Information

Dear Colleagues,

Oxygen is essential for normal aerobic metabolism in mammals. A decreased oxygen concentration in tissues (hypoxia) is a major stressor that generally subverts life and is a prominent feature of pathological states. Therefore, key adaptive mechanisms to cope with hypoxia have evolved in mammals. Additionally, hypoxia is an important pathophysiologic component of many cardiovascular, hematologic and pulmonary disorders and tumor growth.

Cellular responses to hypoxia involve induction of transcription of a network of target genes, a process which is coordinately regulated by hypoxia-inducible transcription factors (HIFs).

An HIF is a heterodimer bHLH transcription factor comprising one of the three oxygen-labile α-subunits (HIF-1α, HIF-2α and HIF-3α) and a constitutively expressed β-subunit (HIFβ—ARNT). The hypoxic microenvironment stabilizes the HIF-α subunit, which is then translocated to the nucleus where it dimerizes with the HIF-β (ARNT) subunit and activates transcription of target genes which promote cell survival. More than 150 genes involved in angiogenesis, glucose metabolism, cell proliferation, survival, apoptosis and invasion/metastasis are activated by HIFs.

As the cellular hypoxic microenvironment is associated with multiple diseases, it is very important to elucidate genes and their expression regulation by HIFs.

This Special Issue is focused on contributing works exploring gene expression changes and regulation mediated by HIFs. We welcome submissions of reviews, research articles, short communications and concept papers.

Dr. Arvydas Kanopka
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. Life is an international peer-reviewed open access monthly 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 2600 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

  • hypoxia
  • HIF
  • chromatin
  • transcription
  • cancer
  • oxygen
  • metabolism

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Published Papers (1 paper)

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Research

19 pages, 1990 KiB  
Article
Cyclosporine A Modulates LSP1 Protein Levels in Human B Cells to Attenuate B Cell Migration at Low O2 Levels
by Shannon P. Hilchey, Mukta G. Palshikar, Eric S. Mendelson, Shichen Shen, Sailee Rasam, Jason A. Emo, Jun Qu, Juilee Thakar and Martin S. Zand
Life 2022, 12(8), 1284; https://doi.org/10.3390/life12081284 - 22 Aug 2022
Cited by 6 | Viewed by 2189
Abstract
Coordinated migration of B cells within and between secondary lymphoid tissues is required for robust antibody responses to infection or vaccination. Secondary lymphoid tissues normally expose B cells to a low O2 (hypoxic) environment. Recently, we have shown that human B cell [...] Read more.
Coordinated migration of B cells within and between secondary lymphoid tissues is required for robust antibody responses to infection or vaccination. Secondary lymphoid tissues normally expose B cells to a low O2 (hypoxic) environment. Recently, we have shown that human B cell migration is modulated by an O2-dependent molecular switch, centrally controlled by the hypoxia-induced (transcription) factor-1α (HIF1A), which can be disrupted by the immunosuppressive calcineurin inhibitor, cyclosporine A (CyA). However, the mechanisms by which low O2 environments attenuate B cell migration remain poorly defined. Proteomics analysis has linked CXCR4 chemokine receptor signaling to cytoskeletal rearrangement. We now hypothesize that the pathways linking the O2 sensing molecular switch to chemokine receptor signaling and cytoskeletal rearrangement would likely contain phosphorylation events, which are typically missed in traditional transcriptomic and/or proteomic analyses. Hence, we have performed a comprehensive phosphoproteomics analysis of human B cells treated with CyA after engagement of the chemokine receptor CXCR4 with CXCL12. Statistical analysis of the separate and synergistic effects of CyA and CXCL12 revealed 116 proteins whose abundance is driven by a synergistic interaction between CyA and CXCL12. Further, we used our previously described algorithm BONITA to reveal a critical role for Lymphocyte Specific Protein 1 (LSP1) in cytoskeletal rearrangement. LSP1 is known to modulate neutrophil migration. Validating these modeling results, we show experimentally that LSP1 levels in B cells increase with low O2 exposure, and CyA treatment results in decreased LSP1 protein levels. This correlates with the increased chemotactic activity observed after CyA treatment. Lastly, we directly link LSP1 levels to chemotactic capacity, as shRNA knock-down of LSP1 results in significantly increased B cell chemotaxis at low O2 levels. These results directly link CyA to LSP1-dependent cytoskeletal regulation, demonstrating a previously unrecognized mechanism by which CyA modulates human B cell migration. Data are available via ProteomeXchange with identifier PXD036167. Full article
(This article belongs to the Special Issue Gene Regulation by HIFs under Hypoxia)
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