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CHAC1 exacerbates arsenite cytotoxicity by lowering intracellular glutathione levels
J Toxicol Sci. 2023;48(9):487-494. doi: 10.2131/jts.48.487.ABSTRACTWe here examined whether CHAC1 is implicated in arsenite (As(III))-induced cytotoxicity in HaCaT cells. We found that HaCaT cells in which the intracellular GSH levels were elevated by transfection with CHAC1 siRNA showed decreased sensitivity to As(III) compared to the control cells. Treatment with BSO (an inhibitor of GSH biosynthesis) abolished the decrease in sensitivity to As(III), suggesting that an increase in intracellular GSH levels was involved in the decrease in sensitivity to As(III) due to the decrease in the levels of CHAC1 expression. When we...
Source: Journal of Toxicological Sciences - September 4, 2023 Category: Toxicology Authors: Daigo Sumi Hiroki Taguchi Kumiko Takeuchi Hitomi Fujishiro Source Type: research

MARCH8 downregulation modulates profibrotic responses including myofibroblast differentiation
In this study, we demonstrated decreased MARCH8 expression in IPF patients compared to non-PF controls and in bleomycin induced PF. TGF-β dose and time dependently decreased MARCH8 expression in normal and IPF human lung fibroblast (HLFs), along with induction of FMT markers α-SMA, collagen type I (Col-1), and fibronectin (FN). Interestingly, overexpression of MARCH8 significantly suppressed TGF-β-induced expression of α-SMA, Col-1, and FN. By contrast, knockdown of MARCH8 using siRNA upregulated basal expression of α-SMA/Col-1/FN. Moreover, MARCH8 knockdown enhanced TGF-β-induced FMT marker expression. These data cl...
Source: American Journal of Physiology. Cell Physiology - September 4, 2023 Category: Cytology Authors: Xia Guo Oluwaseun Adeyanju Ayobami Matthew Olajuyin Venkatakirankumar Mandlem Christudas Sunil Joy Adewumi Steven Huang Torry A Tucker Steven Idell Guoqing Qian Source Type: research

CHAC1 exacerbates arsenite cytotoxicity by lowering intracellular glutathione levels
J Toxicol Sci. 2023;48(9):487-494. doi: 10.2131/jts.48.487.ABSTRACTWe here examined whether CHAC1 is implicated in arsenite (As(III))-induced cytotoxicity in HaCaT cells. We found that HaCaT cells in which the intracellular GSH levels were elevated by transfection with CHAC1 siRNA showed decreased sensitivity to As(III) compared to the control cells. Treatment with BSO (an inhibitor of GSH biosynthesis) abolished the decrease in sensitivity to As(III), suggesting that an increase in intracellular GSH levels was involved in the decrease in sensitivity to As(III) due to the decrease in the levels of CHAC1 expression. When we...
Source: Journal of Toxicological Sciences - September 4, 2023 Category: Toxicology Authors: Daigo Sumi Hiroki Taguchi Kumiko Takeuchi Hitomi Fujishiro Source Type: research

MARCH8 downregulation modulates profibrotic responses including myofibroblast differentiation
In this study, we demonstrated decreased MARCH8 expression in IPF patients compared to non-PF controls and in bleomycin induced PF. TGF-β dose and time dependently decreased MARCH8 expression in normal and IPF human lung fibroblast (HLFs), along with induction of FMT markers α-SMA, collagen type I (Col-1), and fibronectin (FN). Interestingly, overexpression of MARCH8 significantly suppressed TGF-β-induced expression of α-SMA, Col-1, and FN. By contrast, knockdown of MARCH8 using siRNA upregulated basal expression of α-SMA/Col-1/FN. Moreover, MARCH8 knockdown enhanced TGF-β-induced FMT marker expression. These data cl...
Source: Am J Physiol Cell Ph... - September 4, 2023 Category: Cytology Authors: Xia Guo Oluwaseun Adeyanju Ayobami Matthew Olajuyin Venkatakirankumar Mandlem Christudas Sunil Joy Adewumi Steven Huang Torry A Tucker Steven Idell Guoqing Qian Source Type: research

Selective HDAC6 inhibition protects against blood-brain barrier dysfunction after intracerebral hemorrhage
CONCLUSIONS: Inhibition of HDAC6 expression showed beneficial effects against BBB disruption after experimental ICH, which suggested that HDAC6 could be a novel and promising target for ICH treatment.PMID:37665135 | DOI:10.1111/cns.14429
Source: CNS Neuroscience and Therapeutics - September 4, 2023 Category: Neuroscience Authors: Cuiying Peng Yilin Wang Zhiping Hu Chunli Chen Source Type: research

MARCH8 downregulation modulates profibrotic responses including myofibroblast differentiation
In this study, we demonstrated decreased MARCH8 expression in IPF patients compared to non-PF controls and in bleomycin induced PF. TGF-β dose and time dependently decreased MARCH8 expression in normal and IPF human lung fibroblast (HLFs), along with induction of FMT markers α-SMA, collagen type I (Col-1), and fibronectin (FN). Interestingly, overexpression of MARCH8 significantly suppressed TGF-β-induced expression of α-SMA, Col-1, and FN. By contrast, knockdown of MARCH8 using siRNA upregulated basal expression of α-SMA/Col-1/FN. Moreover, MARCH8 knockdown enhanced TGF-β-induced FMT marker expression. These data cl...
Source: American Journal of Physiology. Cell Physiology - September 4, 2023 Category: Cytology Authors: Xia Guo Oluwaseun Adeyanju Ayobami Matthew Olajuyin Venkatakirankumar Mandlem Christudas Sunil Joy Adewumi Steven Huang Torry A Tucker Steven Idell Guoqing Qian Source Type: research

Transcription Factor JunB Suppresses Hepatitis C Virus Replication
Kobe J Med Sci. 2023 Aug 31;69(3):E86-E95.ABSTRACTWe previously reported that hepatitis C virus (HCV) infection activates the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) signaling pathway. Activation of JNK contributes to the development of liver diseases, including metabolic disorders, steatosis, liver cirrhosis and hepatocellular carcinoma. JNK is known to have numerous target genes, including JunB, a member of activator protein-1 transcription factor family. However, the roles of JunB in the HCV life cycle and HCV-associated pathogenesis remain unclear. To clarify a physiological role of JunB in HCV infe...
Source: Kobe J Med Sci - September 4, 2023 Category: General Medicine Authors: Adi Ariffianto Lin Deng Saki Harada Yujiao Liang Chieko Matsui Takayuki Abe Ikuo Shoji Source Type: research

The role of PGRMC2 in the trophoblast invasion
In conclusion, PGRMC2 plays a role in placentation by promoting cell proliferation, invasion, and angiogenesis in EVTs via activation of HIF1α signaling. We thus identified a new function of PGRMC2 and provide insights on understanding the mechanisms of trophoblast invasion.PMID:37665239 | DOI:10.1093/biolre/ioad109
Source: Reproductive Biology - September 4, 2023 Category: Reproduction Medicine Authors: Tae Yokouchi-Konishi Yongjie Liu Liping Feng Source Type: research

MARCH8 downregulation modulates profibrotic responses including myofibroblast differentiation
In this study, we demonstrated decreased MARCH8 expression in IPF patients compared to non-PF controls and in bleomycin induced PF. TGF-β dose and time dependently decreased MARCH8 expression in normal and IPF human lung fibroblast (HLFs), along with induction of FMT markers α-SMA, collagen type I (Col-1), and fibronectin (FN). Interestingly, overexpression of MARCH8 significantly suppressed TGF-β-induced expression of α-SMA, Col-1, and FN. By contrast, knockdown of MARCH8 using siRNA upregulated basal expression of α-SMA/Col-1/FN. Moreover, MARCH8 knockdown enhanced TGF-β-induced FMT marker expression. These data cl...
Source: Am J Physiol Cell Ph... - September 4, 2023 Category: Cytology Authors: Xia Guo Oluwaseun Adeyanju Ayobami Matthew Olajuyin Venkatakirankumar Mandlem Christudas Sunil Joy Adewumi Steven Huang Torry A Tucker Steven Idell Guoqing Qian Source Type: research

Selective HDAC6 inhibition protects against blood-brain barrier dysfunction after intracerebral hemorrhage
CONCLUSIONS: Inhibition of HDAC6 expression showed beneficial effects against BBB disruption after experimental ICH, which suggested that HDAC6 could be a novel and promising target for ICH treatment.PMID:37665135 | DOI:10.1111/cns.14429
Source: CNS Neuroscience and Therapeutics - September 4, 2023 Category: Neuroscience Authors: Cuiying Peng Yilin Wang Zhiping Hu Chunli Chen Source Type: research

Transcription Factor JunB Suppresses Hepatitis C Virus Replication
Kobe J Med Sci. 2023 Aug 31;69(3):E86-E95.ABSTRACTWe previously reported that hepatitis C virus (HCV) infection activates the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) signaling pathway. Activation of JNK contributes to the development of liver diseases, including metabolic disorders, steatosis, liver cirrhosis and hepatocellular carcinoma. JNK is known to have numerous target genes, including JunB, a member of activator protein-1 transcription factor family. However, the roles of JunB in the HCV life cycle and HCV-associated pathogenesis remain unclear. To clarify a physiological role of JunB in HCV infe...
Source: Kobe J Med Sci - September 4, 2023 Category: General Medicine Authors: Adi Ariffianto Lin Deng Saki Harada Yujiao Liang Chieko Matsui Takayuki Abe Ikuo Shoji Source Type: research