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4 results on '"Jiakai Chang"'

1. The therapeutic effect of Shenhua tablet against mesangial cell proliferation and renal inflammation in mesangial proliferative glomerulonephritis

Author

Jiayi He, Fei Peng, Jiakai Chang, Yinghua Zhao, Yilun Qu, Jiaona Liu, Ran Liu, Ping Li, Guangyan Cai, Quan Hong, and Xiangmei Chen

Subjects
Mesangial proliferative glomerulonephritis, Arginine metabolism, ASS1, Inflammation, Network pharmacology, Therapeutics. Pharmacology, RM1-950
Abstract

Shenhua tablet (SH), a formulation of traditional Chinese medicine, exerts renoprotective effect on chronic kidney diseases, and it has been found to restrain inflammation, but the mechanism is still unclear. Here, we explored the potential renoprotection of SH in mesangial proliferative glomerulonephritis (MsPGN) rat model induced by anti-Thy1 antibody. Administration of SH reduced urinary albumin/creatinine ratio (UACR) and significantly attenuated mesangial cell proliferation and renal inflammation. Notably, SH protected rats against renal inflammation, which was associated with decreasing macrophage infiltration and promoting macrophage anti-inflammatory activity. Network analysis combined with arrays identified the Janus kinase signal transducer and activator of transcription (JAK-STAT) signaling pathway as the main pathways of SH could target inflammation. Furthermore, it was confirmed that mesangial cell proliferation, which response to inflammation, were alleviated by ASS1 expression enhanced after SH administration both in vivo and in vitro. Collectively, SH has the beneficial on relieving the progression of MsPGN to alleviate inflammation and mesangial proliferation by inhibiting STAT3 phosphorylation and maintains the expression level of ASS1, might be an effective strategy for treating MsPGN.

Published
2023
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2. Expression characteristics of interferon-stimulated genes and possible regulatory mechanisms in lupus patients using transcriptomics analyses

Author

Yiyao Deng, Ying Zheng, Delun Li, Quan Hong, Min Zhang, Qinggang Li, Bo Fu, Lingling Wu, Xu Wang, Wanjun Shen, Yingjie Zhang, Jiakai Chang, Kangkang Song, Xiaomin Liu, Shunlai Shang, Guangyan Cai, and Xiangmei Chen

Subjects
Single-cell RNA sequencing, Interferon, Granulocytes, Systemic lupus erythematosus, Lupus nephritis, Medicine, Medicine (General), R5-920
Abstract

Background: Type I interferon signature is one of the most important features of systemic lupus erythematosus (SLE), which indicates an active immune response to antigen invasion. Characteristics of type I interferon-stimulated genes (ISGs) in SLE patients have not been well described thus far. Methods: We analyzed 35,842 cells of PBMC single-cell RNA sequencing data of five SLE patients and three healthy controls. Thereafter, 178 type I ISGs among DEGs of all cell clusters were screened based on the Interferome Database and AUCell package was used for ISGs activity calculation. To determine whether common ISG features exist in PBMCs and kidneys of patients with SLE, we analyzed kidney transcriptomic data from patients with lupus nephritis (LN) from the GEO database. MRL/lpr mice model were used to verify our findings. Findings: We found that monocytes, B cells, dendritic cells, and granulocytes were significantly increased in SLE patients, while subsets of T cells were significantly decreased. Neutrophils and low-density granulocytes (LDGs) exhibited the highest ISG activity. GO and pathway enrichment analyses showed that DEGs focused on leukocyte activation, cell secretion, and pathogen infection. Thirty-one common ISGs were found expressed in both PBMCs and kidneys; these ISGs were also most active in neutrophils and LDGs. Transcription factors including PLSCR1, TCF4, IRF9 and STAT1 were found to be associated to ISGs expression. Consistently, we found granulocyte infiltration in the kidneys of MRL/lpr mice. Granulocyte inhibitor Avacopan reduced granulocyte infiltration and reversed renal conditions in MRL/lpr mice. Interpretation: This study shows for the first time, the use of the AUCell method to describe ISG activity of granulocytes in SLE patients. Moreover, Avacopan may serve as a granulocyte inhibitor for treatment of lupus patients in the future.

Published
2021
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3. TGF-β1 peptide-based inhibitor P144 ameliorates renal fibrosis after ischemia-reperfusion injury by modulating alternatively activated macrophages

Author

Delun Li, Jian Zhang, Siyu Yuan, Chao Wang, Jiakai Chang, Yan Tong, Ran Liu, Tian Sang, Lili Li, Jijun Li, Qing Ouyang, and Xiangmei Chen

Subjects
Transforming Growth Factor beta1, Macrophages, Reperfusion Injury, Humans, Kidney Diseases, Cell Biology, General Medicine, Kidney, Fibrosis
Abstract

Ischemia-reperfusion injury (IRI) is a major cause of chronic renal fibrosis. Currently, numerous therapies have shown a minimal effect on the blockade of fibrosis progression. Here, the therapeutic potential of peptide-based TGF-β1 inhibitor P144 in IRI-induced renal fibrosis and the underlying mechanism were analyzed.The unilateral ischemia-reperfusion injury with the contralateral nephrectomy model was established, and the P144 was administered intravenously 1d/14d after the onset of IRI. The histopathology and immunofluorescence staining were used to detect renal fibrosis and macrophage infiltration. The in vivo fluorescence imaging was used to measure the bio-distribution of P144. The transwell assays were used to observe the migration of macrophages. RT-qPCR and western blot were used to analyze TGF-β1 signaling.P144 ameliorated the accumulation of extracellular matrix in the kidney and improved the renal function in the unilateral ischemia-reperfusion injury plus contralateral nephrectomy model. Mechanistically, P144 downregulated the TGF-β1-Smad3 signaling at both the transcriptional and translational levels and further reduced the TGF-β1-dependent infiltration of macrophages to the injured kidney. Additionally, P144 blocked the polarization of macrophages to an M2-like phenotype induced by TGF-β1 in vitro, but showed no effect on their proliferation.Our study showed that the TGF-β1 peptide-based inhibitor P144 decreased renal fibrosis through the blockade of the TGF-β1-Smad3 signaling pathway and the modulation of macrophage polarization, suggesting its potential therapeutic use in IRI-induced renal fibrosis.

Published
2022

4. Expression characteristics of interferon-stimulated genes and possible regulatory mechanisms in lupus patients using transcriptomics analyses

Author

Bo Fu, Quan Hong, Xiaomin Liu, Qinggang Li, Kangkang Song, Min Zhang, Jiakai Chang, Guangyan Cai, Wanjun Shen, Shunlai Shang, Yingjie Zhang, Yiyao Deng, Xu Wang, Ying Zheng, Lingling Wu, De-Lun Li, and Xiangmei Chen

Subjects
Medicine (General), Lupus nephritis, Biology, Granulocyte, Kidney, Peripheral blood mononuclear cell, General Biochemistry, Genetics and Molecular Biology, Transcriptome, Single-cell RNA sequencing, Mice, R5-920, Systemic lupus erythematosus, Transcription Factor 4, Antigen, Interferon, immune system diseases, medicine, Animals, Humans, Lupus Erythematosus, Systemic, STAT1, Phospholipid Transfer Proteins, skin and connective tissue diseases, virus diseases, General Medicine, medicine.disease, Interferon-Stimulated Gene Factor 3, gamma Subunit, Mice, Inbred C57BL, medicine.anatomical_structure, STAT1 Transcription Factor, Immunology, biology.protein, Leukocytes, Mononuclear, Medicine, Female, Interferons, medicine.drug, Research Paper, Granulocytes
Abstract

Background Type I interferon signature is one of the most important features of systemic lupus erythematosus (SLE), which indicates an active immune response to antigen invasion. Characteristics of type I interferon-stimulated genes (ISGs) in SLE patients have not been well described thus far. Methods We analyzed 35,842 cells of PBMC single-cell RNA sequencing data of five SLE patients and three healthy controls. Thereafter, 178 type I ISGs among DEGs of all cell clusters were screened based on the Interferome Database and AUCell package was used for ISGs activity calculation. To determine whether common ISG features exist in PBMCs and kidneys of patients with SLE, we analyzed kidney transcriptomic data from patients with lupus nephritis (LN) from the GEO database. MRL/lpr mice model were used to verify our findings. Findings We found that monocytes, B cells, dendritic cells, and granulocytes were significantly increased in SLE patients, while subsets of T cells were significantly decreased. Neutrophils and low-density granulocytes (LDGs) exhibited the highest ISG activity. GO and pathway enrichment analyses showed that DEGs focused on leukocyte activation, cell secretion, and pathogen infection. Thirty-one common ISGs were found expressed in both PBMCs and kidneys; these ISGs were also most active in neutrophils and LDGs. Transcription factors including PLSCR1, TCF4, IRF9 and STAT1 were found to be associated to ISGs expression. Consistently, we found granulocyte infiltration in the kidneys of MRL/lpr mice. Granulocyte inhibitor Avacopan reduced granulocyte infiltration and reversed renal conditions in MRL/lpr mice. Interpretation This study shows for the first time, the use of the AUCell method to describe ISG activity of granulocytes in SLE patients. Moreover, Avacopan may serve as a granulocyte inhibitor for treatment of lupus patients in the future. Funding None.

Published
2021

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