NDLI: Molecular Mechanisms Regulating Macrophage Response to Hypoxia

Content Provider	PubMed Central
Author	Rahat, Michal A. Bitterman, Haim Lahat, Nitza
Copyright Year	2011
Abstract	Monocytes and Macrophages (Mo/Mɸ) exhibit great plasticity, as they can shift between different modes of activation and, driven by their immediate microenvironment, perform divergent functions. These include, among others, patrolling their surroundings and maintaining homeostasis (resident Mo/Mɸ), combating invading pathogens and tumor cells (classically activated or M1 Mo/Mɸ), orchestrating wound healing (alternatively activated or M2 Mo/Mɸ), and restoring homeostasis after an inflammatory response (resolution Mɸ). Hypoxia is an important factor in the Mɸ microenvironment, is prevalent in many physiological and pathological conditions, and is interdependent with the inflammatory response. Although Mo/Mɸ have been studied in hypoxia, the mechanisms by which hypoxia influences the different modes of their activation, and how it regulates the shift between them, remain unclear. Here we review the current knowledge about the molecular mechanisms that mediate this hypoxic regulation of Mɸ activation. Much is known about the hypoxic transcriptional regulatory network, which includes the master regulators hypoxia-induced factor-1 and NF-κB, as well as other transcription factors (e.g., AP-1, Erg-1), but we also highlight the role of post-transcriptional and post-translational mechanisms. These mechanisms mediate hypoxic induction of Mɸ pro-angiogenic mediators, suppress M1 Mɸ by post-transcriptionally inhibiting pro-inflammatory mediators, and help shift the classically activated Mɸ into an activation state which approximate the alternatively activated or resolution Mɸ.
Related Links	http://dx.doi.org/10.3389/fimmu.2011.00045
Starting Page	45
File Format	PDF
ISSN	16643224
e-ISSN	16643224
Journal	Frontiers in Immunology
Volume Number	2
Language	English
Publisher	Frontiers Research Foundation
Publisher Date	2011-01-01
Access Restriction	Open
Rights Holder	Frontiers Research Foundation
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Akt1 controls macrophage response to LPS by regulating microRNAs

Molecular mechanisms regulating CD13-mediated adhesion

Crosstalk Between Hypoxia and ER Stress Response: A Key Regulator of Macrophage Polarization

Molecular mechanisms regulating myeloid-derived suppressor cell differentiation and function

Molecular mechanisms regulating NLRP3 inflammasome activation

Molecular Mechanisms Regulating TGF-β-Induced Foxp3 Expression

IL-18 contributes to susceptibility to Leishmania amazonensis infection by macrophage-independent mechanisms

Molecular mechanisms regulating NETosis in infection and disease

Molecular Mechanisms Regulating Cytotoxic Lymphocyte Development and Function, and Their Associations to Human Diseases

Molecular Mechanisms Regulating Macrophage Response to Hypoxia

Similar Documents

Akt1 controls macrophage response to LPS by regulating microRNAs

Molecular mechanisms regulating CD13-mediated adhesion

Crosstalk Between Hypoxia and ER Stress Response: A Key Regulator of Macrophage Polarization

Molecular mechanisms regulating myeloid-derived suppressor cell differentiation and function

Molecular mechanisms regulating NLRP3 inflammasome activation

Molecular Mechanisms Regulating TGF-β-Induced Foxp3 Expression

IL-18 contributes to susceptibility to Leishmania amazonensis infection by macrophage-independent mechanisms

Molecular mechanisms regulating NETosis in infection and disease

Molecular Mechanisms Regulating Cytotoxic Lymphocyte Development and Function, and Their Associations to Human Diseases

Molecular Mechanisms Regulating Macrophage Response to Hypoxia