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Inhibition of lactate dehydrogenase A suppresses inflammatory response in RAW 264.7 macrophages

Authors
Song, Yoo-JeongKim, AhyeonKim, Goon-TaeYu, Han YoungLee, Eun-SoPark, Mi JinKim, Young-JunShim, Soon-MiPark, Tae-Sik
Issue Date
1월-2019
Publisher
SPANDIDOS PUBL LTD
Keywords
lactate; inflammation; lactate dehydrogenase; mitogen-activated protein kinase; cytokines
Citation
MOLECULAR MEDICINE REPORTS, v.19, no.1, pp.629 - 637
Indexed
SCIE
SCOPUS
Journal Title
MOLECULAR MEDICINE REPORTS
Volume
19
Number
1
Start Page
629
End Page
637
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/68793
DOI
10.3892/mmr.2018.9678
ISSN
1791-2997
Abstract
Lactate is an important metabolite in cellular metabolism and fluctuates in certain disease conditions including cancer and immune diseases. It was hypothesized that a decrease in lactate would modulate the inflammatory response elicited by lipopolysaccharides (LPS) in macrophages. When RAW 264.7 macrophages were treated with FX11, a specific lactate dehydrogenase (LDHA) inhibitor, the expression of the cytokines, inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) was downregulated due to reduced cellular lactate levels. Genetic suppression of LDHA by small interfering RNA (siRNA) downregulated the LPS-activated expression of interleukin (IL)-6, iNOS, and COX-2, and reduced the production of IL-6 and nitrites. Pharmacological and genetic suppression of LDHA inhibited the phosphorylation of p38 mitogen-activated protein kinase. Microarray gene expression profile demonstrated that the genes involved in cell proliferation and inflammation were mainly altered by siRNA-mediated LDHA suppression. Collectively, the present observations suggest that lactate may be an important metabolite and implicated in regulation of inflammatory response.
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