Quantitative Proteomic Profiling of Renal Tissue in Human Chronic Rejection Biopsy Samples After Renal Transplantation

Lin, Xiuhua; Sui, Weiguo; Qi, Suwen; Tang, Donge; Cong, Shan; Zou, Guimian; Zhang, Y.; Li, H.; Chen, Wei Bo; Cheng, Zhiqiang; Dai, Yong

doi:10.1016/j.transproceed.2014.10.010

Cited by 5 publications

(7 citation statements)

References 30 publications

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“…We compared the differences in the levels of the isolated proteins from ALV-J-infected and mock-infected DF-1 cells by quantitative proteomics. Using a strict cutoff value of 1.5-fold for expressed variation 24 and using the GO function significant sexual enrichment analysis, we found some differentially expressed proteins involved in the MAPK signaling pathway ( Fig. 1 ).…”

Section: Resultsmentioning

confidence: 99%

Exogenous avian leukosis virus-induced activation of the ERK/AP1 pathway is required for virus replication and correlates with virus-induced tumorigenesis

Dai

Feng

et al. 2016

Sci Rep

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A proteomics approach was used to reveal the up-regulated proteins involved in the targeted mitogen-activated protein kinase (MAPK) signal transduction pathway in DF-1 cells after ALV subgroup J (ALV-J) infection. Next, we found that ALV-J CHN06 strain infection of DF-1 cells correlated with extracellular signal-regulated kinase 2 (ERK2) activation, which was mainly induced within 15 min, a very early stage of infection, and at a late infection stage, from 108 h to 132 h post-infection. Infection with other ALV subgroup (A/B) strains also triggered ERK/MAPK activation. Moreover, when activating ERK2, ALV subgroups A, B and J simultaneously induced the phosphorylation of c-Jun, an AP1 family member and p38 activation but had no obvious effect on JNK activation at either 15 min or 120 h. Interestingly, only PD98059 inhibited the ALV-induced c-Jun phosphorylation while SP600125 or SB203580 had no influence on c-Jun activation. Furthermore, the viral gp85 and gag proteins were found to contribute to ERK2/AP1 activation. Additionally, the specific ERK inhibitor, PD980509, significantly suppressed ALV replication, as evidenced by extremely low levels of ALV promoter activity and ALV-J protein expression. In vivo analysis of ERK2 activation in tumor cells derived from ALV-J-infected chicken demonstrated a strong correlation between ERK/MAPK activation and virus-associated tumorigenesis.

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Section: Resultsmentioning

confidence: 99%

Exogenous avian leukosis virus-induced activation of the ERK/AP1 pathway is required for virus replication and correlates with virus-induced tumorigenesis

Dai

Feng

et al. 2016

Sci Rep

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“…ITRAQ labeling was performed using the 8-plex iTRAQ reagents (Applied Biosystems, Foster City, CA, USA) as previously reported [ 49 ]. Then, the labeled samples were lyophilized and assigned to HPLC-MS/MS (high performance liquid chromatography-mass spectrometry/ mass spectrometry) analysis in HPLC electrospray ionization MS/MS system (Applied Biosystems, Foster City, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

Multi-omics analysis reveals regulators of the response to PDGF-BB treatment in pulmonary artery smooth muscle cells

et al. 2016

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BackgroundPulmonary arterial hypertension (PAH) is a lethal disease with pronounced narrowing of pulmonary vessels due to abnormal cell proliferation. The platelet-derived growth factor BB (PDGF-BB) is well known as a potent mitogen for smooth muscle cell proliferation. To better understand how this growth factor regulates pulmonary arterial smooth muscle cells (PASMCs) proliferation, we sought to characterize the response to PDGF-BB stimulation at system-wide levels, including the transcriptome and proteome.ResultsIn this study, we identified 1611 mRNAs (transcriptome), 207 proteins (proteome) differentially expressed in response to PDGF-BB stimulation in PASMCs based on RNA-sequencing and isobaric tags for relative and absolute quantification (iTRAQ) assay. Transcription factor (TF)-target network analysis revealed that PDGF-BB regulated gene expression potentially via TFs including HIF1A, JUN, EST1, ETS1, SMAD1, FOS, SP1, STAT1, LEF1 and CEBPB. Among them, SMAD1-involved BMPR2/SMADs axis plays a significant role in PAH development. Interestingly, we observed that the expression of BMPR2 was decreased in both mRNA and protein level in response to PDGF-BB. Further study revealed that BMPR2 is the direct target of miR-376b that is up-regulated upon PDGF-BB treatment. Finally, EdU incorporation assay showed that miR-376b promoted proliferation of PASMCs.ConclusionThis integrated analysis of PDGF-BB-regulated transcriptome and proteome was performed for the first time in normal PASMCs, which revealed a crosstalk between PDGF signaling and BMPR2/SMADs axis. Further study demonstrated that PDGF-BB-induced miR-376b upregulation mediated the downregulation of BMPR2, which led to expression change of its downstream targets and promoted proliferation of PASMCs.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-3122-3) contains supplementary material, which is available to authorized users.

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“…Two examples of proteomic studies, including renal biopsies of transplanted patients, were conducted by Nakorchevsky et al and Lin et al [ 11 , 41 ]. The former evaluated 33 biopsies from individuals with CR and diverse degrees of IFTA, whereas the latter analyzed 19 biopsies to discriminate between CR and renal adenocarcinoma.…”

Section: Why Proteomics?mentioning

confidence: 99%

“…Nakorchevsky et al [ 11 ] observed 492 unique proteins related to the progression from normal to mild, to moderate, and severe disease, including proteins associated with immune responses, inflammatory cell activation, and apoptosis. Meanwhile, Lin et al [ 41 ] observed that 87 out of 1587 identified proteins were 1.5-fold higher in CR in relation to adenocarcinoma. There are also diverse proteomics studies focusing on urine and plasma/serum proteome to predict kidney function [ 42 ], including in patients with cancer [ 43 , 44 ] and diabetes [ 45 ].…”

Section: Why Proteomics?mentioning

confidence: 99%

Proteomics for Biomarker Discovery for Diagnosis and Prognosis of Kidney Transplantation Rejection

et al. 2022

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Renal transplantation is currently the treatment of choice for end-stage kidney disease, enabling a quality of life superior to dialysis. Despite this, all transplanted patients are at risk of allograft rejection processes. The gold-standard diagnosis of graft rejection, based on histological analysis of kidney biopsy, is prone to sampling errors and carries high costs and risks associated with such invasive procedures. Furthermore, the routine clinical monitoring, based on urine volume, proteinuria, and serum creatinine, usually only detects alterations after graft histologic damage and does not differentiate between the diverse etiologies. Therefore, there is an urgent need for new biomarkers enabling to predict, with high sensitivity and specificity, the rejection processes and the underlying mechanisms obtained from minimally invasive procedures to be implemented in routine clinical surveillance. These new biomarkers should also detect the rejection processes as early as possible, ideally before the78 clinical outputs, while enabling balanced immunotherapy in order to minimize rejections and reducing the high toxicities associated with these drugs. Proteomics of biofluids, collected through non-invasive or minimally invasive analysis, e.g., blood or urine, present inherent characteristics that may provide biomarker candidates. The current manuscript reviews biofluids proteomics toward biomarkers discovery that specifically identify subclinical, acute, and chronic immune rejection processes while allowing for the discrimination between cell-mediated or antibody-mediated processes. In time, these biomarkers will lead to patient risk stratification, monitoring, and personalized and more efficient immunotherapies toward higher graft survival and patient quality of life.

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Quantitative Proteomic Profiling of Renal Tissue in Human Chronic Rejection Biopsy Samples After Renal Transplantation

Cited by 5 publications

References 30 publications

Exogenous avian leukosis virus-induced activation of the ERK/AP1 pathway is required for virus replication and correlates with virus-induced tumorigenesis

Exogenous avian leukosis virus-induced activation of the ERK/AP1 pathway is required for virus replication and correlates with virus-induced tumorigenesis

Multi-omics analysis reveals regulators of the response to PDGF-BB treatment in pulmonary artery smooth muscle cells

Proteomics for Biomarker Discovery for Diagnosis and Prognosis of Kidney Transplantation Rejection

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