TY - JOUR
T1 - Expression profiles of genes associated with inflammatory responses and oxidative stress in lung after heat stroke
AU - Liu, Zhaoyu
AU - Chen, Jitao
AU - Hu, La
AU - Li, Ming
AU - Liang, Min
AU - Chen, Jianan
AU - Lin, Hai
AU - Zeng, Zicheng
AU - Yin, Weida
AU - Dong, Zhijie
AU - Weng, Jinsheng
AU - Yao, Wenxia
AU - Yi, Gao
N1 - Funding Information:
This research program was financially sponsored by the National Natural Science Foundation of China [grant numbers 81873419, 81400013 and 81570189]; Natural Science Foundation of Guangdong Province [grant number 2018A030313587]; and Science and Technology Program of Guangzhou, China [grant number 201804010018]. This work was completed in the Central Laboratory of the Fifth Affiliated Hospital of Guangzhou Medical University.
Publisher Copyright:
© 2020 The Author(s).
PY - 2020/6
Y1 - 2020/6
N2 - Background: Heat stroke (HS) is a physically dysfunctional illness caused by hyperthermia. Lung, as the important place for gas-exchange and heat-dissipation organ, is often first to be injured. Lung injury caused by HS impairs the ventilation function of lung, which will subsequently cause damage to other tissues and organs. Nevertheless, the specific mechanism of lung injury in heat stroke is still unknown. Methods: Rat lung tissues from controls or HS models were harvested. The gene expression profile was identified by high-throughput sequencing. DEGs were calculated using R and validated by qRT-PCR. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and cell-enrichment were performed using differential expression genes (DEGs). Finally, lung histopathology was accessed by H&E staining. Results: About 471 genes were identified to be DEGs, of which 257 genes were up-regulated, and 214 genes were down-regulated. The most up-regulated and down-regulated DEGs were validated by qRT-PCR, which confirmed the tendency of expression. GO, KEGG, and protein–protein interaction (PPI)-network analyses disclosed DEGs were significantly enriched in leukocyte migration, response to lipopolysaccharide, NIK/NF-kappaB signaling, response to reactive oxygen species, response to heat, and the hub genes were Tnf, Il1b, Cxcl2, Ccl2, Mmp9, Timp1, Hmox1, Serpine1, Mmp8 and Csf1, most of which were closely related to inflammagenesis and oxidative stress. Finally, cell-enrichment analysis and histopathologic analysis showed Monocytes, Megakaryotyes, and Macrophages were enriched in response to heat stress. Conclusions: The present study identified key genes, signal pathways and infiltrated-cell types in lung after heat stress, which will deepen our understanding of transcriptional response to heat stress, and might provide new ideas for the treatment of HS.
AB - Background: Heat stroke (HS) is a physically dysfunctional illness caused by hyperthermia. Lung, as the important place for gas-exchange and heat-dissipation organ, is often first to be injured. Lung injury caused by HS impairs the ventilation function of lung, which will subsequently cause damage to other tissues and organs. Nevertheless, the specific mechanism of lung injury in heat stroke is still unknown. Methods: Rat lung tissues from controls or HS models were harvested. The gene expression profile was identified by high-throughput sequencing. DEGs were calculated using R and validated by qRT-PCR. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and cell-enrichment were performed using differential expression genes (DEGs). Finally, lung histopathology was accessed by H&E staining. Results: About 471 genes were identified to be DEGs, of which 257 genes were up-regulated, and 214 genes were down-regulated. The most up-regulated and down-regulated DEGs were validated by qRT-PCR, which confirmed the tendency of expression. GO, KEGG, and protein–protein interaction (PPI)-network analyses disclosed DEGs were significantly enriched in leukocyte migration, response to lipopolysaccharide, NIK/NF-kappaB signaling, response to reactive oxygen species, response to heat, and the hub genes were Tnf, Il1b, Cxcl2, Ccl2, Mmp9, Timp1, Hmox1, Serpine1, Mmp8 and Csf1, most of which were closely related to inflammagenesis and oxidative stress. Finally, cell-enrichment analysis and histopathologic analysis showed Monocytes, Megakaryotyes, and Macrophages were enriched in response to heat stress. Conclusions: The present study identified key genes, signal pathways and infiltrated-cell types in lung after heat stress, which will deepen our understanding of transcriptional response to heat stress, and might provide new ideas for the treatment of HS.
UR - http://www.scopus.com/inward/record.url?scp=85086052223&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85086052223&partnerID=8YFLogxK
U2 - 10.1042/BSR20192048
DO - 10.1042/BSR20192048
M3 - Article
C2 - 32436952
AN - SCOPUS:85086052223
SN - 0144-8463
VL - 40
JO - Bioscience reports
JF - Bioscience reports
IS - 6
M1 - BSR20192048
ER -