Sodium butyrate impedes the lymphoma caused by Marek’s disease virus via regulating the mitochondrial apoptosis pathway

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Sodium butyrate (NaB) has garnered attention in recent years for its ability to impede the malignant progression of tumors. In order to explore the potential inhibitory effects of NaB on the replication of Marek’s disease virus (MDV) and subsequent lymphoma formation, newly hatched chickens were infected with the vvMDV Md5 strain and administered NaB prior to (prevention group) or following (treatment group) Md5 inoculation. The results revealed that NaB played a pivotal role in diminishing both the incidence and fatality rates in chickens afflicted with Md5 infection. Notably, NaB exhibited a remarkable capacity to inhibit the expression of MDV immediate early genes, i.e., ICP4 and ICP27, thus attenuating tumorigenesis in the chicken spleen. To further elucidate the mechanism of NaB on lymphoma cells, MDV bearing lymphoma cells, i.e., MSB-1 were exposed to NaB for 24 h prior to various experimental tests. The results revealed that NaB effectively hindered the proliferation, migration, and colony formation of MSB-1 cells. Furthermore, NaB demonstrated the ability to modulate the key molecules in mitochondrial apoptosis pathway. Taken together, these findings reveal that NaB can impede the lymphoma caused by MDV via regulating the mitochondrial apoptosis pathway, both in vitro and in vivo. These results suggest that the utilization of NaB warrants serious consideration as a promising approach for the prevention of MDV.

Related collections

Most cited references 65

Record: found
Abstract: found
Article: found

Is Open Access

Short Chain Fatty Acids (SCFAs)-Mediated Gut Epithelial and Immune Regulation and Its Relevance for Inflammatory Bowel Diseases

Daniela Parada Venegas, Marjorie K. De la Fuente, Glauben Landskron … (2019)

Ulcerative colitis (UC) and Crohn's disease (CD), collectively known as Inflammatory Bowel Diseases (IBD), are caused by a complex interplay between genetic, immunologic, microbial and environmental factors. Dysbiosis of the gut microbiome is increasingly considered to be causatively related to IBD and is strongly affected by components of a Western life style. Bacteria that ferment fibers and produce short chain fatty acids (SCFAs) are typically reduced in mucosa and feces of patients with IBD, as compared to healthy individuals. SCFAs, such as acetate, propionate and butyrate, are important metabolites in maintaining intestinal homeostasis. Several studies have indeed shown that fecal SCFAs levels are reduced in active IBD. SCFAs are an important fuel for intestinal epithelial cells and are known to strengthen the gut barrier function. Recent findings, however, show that SCFAs, and in particular butyrate, also have important immunomodulatory functions. Absorption of SCFAs is facilitated by substrate transporters like MCT1 and SMCT1 to promote cellular metabolism. Moreover, SCFAs may signal through cell surface G-protein coupled receptors (GPCRs), like GPR41, GPR43, and GPR109A, to activate signaling cascades that control immune functions. Transgenic mouse models support the key role of these GPCRs in controlling intestinal inflammation. Here, we present an overview of microbial SCFAs production and their effects on the intestinal mucosa with specific emphasis on their relevance for IBD. Moreover, we discuss the therapeutic potential of SCFAs for IBD, either applied directly or by stimulating SCFAs-producing bacteria through pre- or probiotic approaches.

0 comments Cited 1098 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy.

S Fulda, K-M Debatin (2006)

Apoptosis or programmed cell death is a key regulator of physiological growth control and regulation of tissue homeostasis. One of the most important advances in cancer research in recent years is the recognition that cell death mostly by apoptosis is crucially involved in the regulation of tumor formation and also critically determines treatment response. Killing of tumor cells by most anticancer strategies currently used in clinical oncology, for example, chemotherapy, gamma-irradiation, suicide gene therapy or immunotherapy, has been linked to activation of apoptosis signal transduction pathways in cancer cells such as the intrinsic and/or extrinsic pathway. Thus, failure to undergo apoptosis may result in treatment resistance. Understanding the molecular events that regulate apoptosis in response to anticancer chemotherapy, and how cancer cells evade apoptotic death, provides novel opportunities for a more rational approach to develop molecular-targeted therapies for combating cancer.

0 comments Cited 617 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Chemical inhibition of the mitochondrial division dynamin reveals its role in Bax/Bak-dependent mitochondrial outer membrane permeabilization.

Ann Cassidy-Stone, Jerry E Chipuk, Elena Ingerman … (2008)

Mitochondrial fusion and division play important roles in the regulation of apoptosis. Mitochondrial fusion proteins attenuate apoptosis by inhibiting release of cytochrome c from mitochondria, in part by controlling cristae structures. Mitochondrial division promotes apoptosis by an unknown mechanism. We addressed how division proteins regulate apoptosis using inhibitors of mitochondrial division identified in a chemical screen. The most efficacious inhibitor, mdivi-1 (for mitochondrial division inhibitor) attenuates mitochondrial division in yeast and mammalian cells by selectively inhibiting the mitochondrial division dynamin. In cells, mdivi-1 retards apoptosis by inhibiting mitochondrial outer membrane permeabilization. In vitro, mdivi-1 potently blocks Bid-activated Bax/Bak-dependent cytochrome c release from mitochondria. These data indicate the mitochondrial division dynamin directly regulates mitochondrial outer membrane permeabilization independent of Drp1-mediated division. Our findings raise the interesting possibility that mdivi-1 represents a class of therapeutics for stroke, myocardial infarction, and neurodegenerative diseases.

0 comments Cited 412 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

Qiaoer Lin: Role: Role: Role: Role: Role: Role:

Jun Zhou: Role: Role: Role: Role:

Fan Yang: Role: Role: Role: Role: Role:

Congsen Zheng: Role: Role: Role: Role:

Meiting Chen: Role: Role: Role:

Chuanzhe Chang: Role: Role: Role:

Shikai Cai: Role: Role:

Feng Wen: URI : https://loop.frontiersin.org/people/1066918/overviewRole:

Nina Wang: URI : https://loop.frontiersin.org/people/1091468/overviewRole:

Yanfeng Chen: Role:

Limei Qin: URI : https://loop.frontiersin.org/people/2612460/overviewRole: Role: Role: Role:

Journal

Journal ID (nlm-ta): Front Vet Sci

Journal ID (iso-abbrev): Front Vet Sci

Journal ID (publisher-id): Front. Vet. Sci.

Title: Frontiers in Veterinary Science

Publisher: Frontiers Media S.A.

ISSN (Electronic): 2297-1769

Publication date (Electronic): 28 February 2024

Publication date Collection: 2024

Volume: 11

Electronic Location Identifier: 1360878

Affiliations

[1] ¹School of Life Science and Engineering, Foshan University , Foshan, China

[2] ²Guangdong Provincial Key Laboratory of Animal Molecular Design and Precise Breeding, Foshan University , Foshan, China

Author notes

Edited by: Marxa L. Figueiredo, Purdue University, United States

Reviewed by: Kishor Pant, University of Minnesota Twin Cities, United States

Daryoush Babazadeh, Shiraz University, Iran

*Correspondence: Limei Qin, qlm@ 123456fosu.edu.cn

^†These authors have contributed equally to this work

Article

DOI: 10.3389/fvets.2024.1360878

PMC ID: 10932986

PubMed ID: 38482171

SO-VID: 9be2392e-c3c9-4990-b99e-10421022035f

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

History

Date received : 24 December 2023

Date accepted : 15 February 2024

Page count

Figures: 11, Tables: 2, Equations: 0, References: 65, Pages: 15, Words: 8297

Funding

The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. This research was funded by Guangdong Basic and Applied Basic Research Foundation (2021A1515012388) and the Guangdong Provincial Key Laboratory of Animal Molecular Design and Precise Breeding (2019B030301010).

Custom metadata

section-at-acceptance Oncology in Veterinary Medicine

Keywords: sodium butyrate,lymphoma,apoptosis,mitochondrion,mdv,latency,icp4

Data availability:

Keywords: sodium butyrate, lymphoma, apoptosis, mitochondrion, mdv, latency, icp4

Sodium butyrate impedes the lymphoma caused by Marek’s disease virus via regulating the mitochondrial apoptosis pathway

Read this article at

Abstract

Related collections

Alternative approaches to Alzheimer's Disease

Most cited references 65

Short Chain Fatty Acids (SCFAs)-Mediated Gut Epithelial and Immune Regulation and Its Relevance for Inflammatory Bowel Diseases

Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy.

Chemical inhibition of the mitochondrial division dynamin reveals its role in Bax/Bak-dependent mitochondrial outer membrane permeabilization.

Author and article information

Contributors

Journal

Affiliations

Author notes

Article

History

Page count

Funding

Categories

Custom metadata

Comments

Comment on this article

Similar content 203

Most referenced authors 819