Xin J. Zhou

ORCID: 0000-0002-1617-334X
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About
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Research Areas
  • Systemic Lupus Erythematosus Research
  • T-cell and B-cell Immunology
  • Renal Diseases and Glomerulopathies
  • Dialysis and Renal Disease Management
  • Acute Kidney Injury Research
  • Immune Cell Function and Interaction
  • Sperm and Testicular Function
  • Chemokine receptors and signaling
  • Monoclonal and Polyclonal Antibodies Research
  • Chronic Kidney Disease and Diabetes
  • Immune Response and Inflammation
  • Growth Hormone and Insulin-like Growth Factors
  • Reproductive Biology and Fertility
  • Renin-Angiotensin System Studies
  • Atherosclerosis and Cardiovascular Diseases
  • Pituitary Gland Disorders and Treatments
  • Nitric Oxide and Endothelin Effects
  • Birth, Development, and Health
  • Lymphoma Diagnosis and Treatment
  • Metabolism, Diabetes, and Cancer
  • CNS Lymphoma Diagnosis and Treatment
  • Renal function and acid-base balance
  • Thyroid Disorders and Treatments
  • Muscle and Compartmental Disorders
  • Erythropoietin and Anemia Treatment

Umeå University
2023-2025

Qingdao University
2025

Gansu University of Traditional Chinese Medicine
2020

The University of Texas Southwestern Medical Center
2005-2015

Pathologist Bio-Medical Laboratories
2015

Baylor University Medical Center
2015

Nanjing General Hospital of Nanjing Military Command
2010

Southwestern Medical Center
2009

Chinese PLA General Hospital
2003

National University of Singapore
1997-2001

The y-linked autoimmune accelerating (yaa) locus is a potent disease allele. Transcription profiling of yaa-bearing B cells revealed the overexpression cluster X-linked genes that included Tlr7. FISH analysis demonstrated translocation this segment onto yaa chromosome. resulting Tlr7 increased in vitro responses to Toll-like receptor (TLR) 7 signaling all males. B6.yaa mice are not overtly autoimmune, but addition Sle1, which contains autoimmune-predisposing Slam/Cd2 haplotype, causes...

10.1073/pnas.0603912103 article EN Proceedings of the National Academy of Sciences 2006-06-15

The role of IL-6 was investigated in murine ischemic acute renal failure. pedicles were clamped for 17 min, and the mice studied at various times after reperfusion. We found that serum increased injury. This increase associated with mRNA kidney but not contralateral or liver. Maximal production occurred 4 to 8 h decreased baseline by 24 h. Reperfusion required production. In situ hybridization immunohistochemistry showed macrophages infiltrated areas adjacent vascular bundles outer medulla...

10.1681/asn.2003090757 article EN Journal of the American Society of Nephrology 2005-09-29

A combined forward and reverse genetic approach was undertaken to test the candidacy of IRAK1 (interleukin-1 receptor associated kinase-1) as an X chromosome-encoded risk factor for systemic lupus erythematosus (SLE). In studying approximately 5,000 subjects healthy controls, 5 SNPs spanning gene showed disease association (P values reaching 10(-10), odds ratio >1.5) in both adult- childhood-onset SLE, 4 different ethnic groups, with a SNP haplotype (GGGG) being strongly disease. The...

10.1073/pnas.0901181106 article EN Proceedings of the National Academy of Sciences 2009-03-30

Abstract In an effort to identify potential biomarkers in lupus nephritis, urine from mice with spontaneous nephritis was screened for the presence of VCAM-1, P-selectin, TNFR-1, and CXCL16, four molecules that had previously been shown be elevated experimental immune particularly at peak disease. Interestingly, all were ∼2- 4-fold several strains including MRL/lpr, NZM2410, B6.Sle1.lpr strains, correlating well proteinuria. CXCL16 enriched compared serum active disease, expressed within...

10.4049/jimmunol.179.10.7166 article EN The Journal of Immunology 2007-11-15

The Y-linked autoimmune accelerating (Yaa) locus drives the transition to fatal lupus nephritis when combined with B6.Sle1 in our C57BL/6J (B6)-congenic model of systemic autoimmunity. We and others recently demonstrated that translocation a cluster X-linked genes onto Y chromosome is genetic lesion underlying Yaa (Subramanian, S. et al., Proc. Natl. Acad. Sci. USA 2006. 103: 9970-9975; Pisitkun, P. Science 312: 1669-1672). In male mice carrying Yaa, transcription several within translocated...

10.1002/eji.200838138 article EN European Journal of Immunology 2008-06-03

Redox‐based diagnostic and therapeutic applications have long suffered from a shortage of suitable drugs probes high specificity. In the context anti‐ferroptosis research for neurological diseases, inaccessibility blood‐brain barrier permeable (BBB) small molecular ferroptosis inhibitor, lack specific seriously impeded deeper understanding mechanism development clinically applicable drugs. We here report novel 1,3,4‑thiadiazole‐functionalized drug‐like ferrostatin analogue entitled...

10.1002/anie.202502195 article EN Angewandte Chemie International Edition 2025-02-21

Kidneys of newborn (but not adult) mice are normally high permissive for polyomavirus (Py) infection and readily establish persistent infections. We have proposed that ongoing cellular differentiation, which occurs in mice, may be necessary a level vivo Py replication (R. Rochford, J. P. Moreno, M. L. Peake, Villarreal, Virol. 66:3287-3297, 1992). This differentiation requirement also the reactivation kidney could provide an alternative to accepted view results from immunosuppression. To...

10.1128/jvi.67.3.1424-1432.1993 article EN Journal of Virology 1993-03-01

Immune-mediated nephritis contributes to disease in systemic lupus erythematosus, Goodpasture syndrome (caused by antibodies specific for glomerular basement membrane [anti-GBM antibodies]), and spontaneous nephritis. Inbred mouse strains differ susceptibility anti-GBM antibody-induced This study sought clarify the genetic molecular factors that maybe responsible enhanced immune-mediated renal these models. When kidneys of 3 sensitive were compared with those 2 control using microarray...

10.1172/jci36728 article EN Journal of Clinical Investigation 2009-04-01

Among various surface molecules screened, CXCR4 was significantly up-regulated on monocytes, neutrophils, B cell subsets, and plasma cells in multiple murine models of lupus with active nephritis, including B6.Sle1Yaa, BXSB, MRL.lpr. TLR-mediated signaling inflammatory cytokines accounted part for this increase. Increased expression associated functional consequences, increased migration enhanced survival. Simultaneously, the ligand CXCR4, CXCL12, nephritic kidneys. Treatment a peptide...

10.4049/jimmunol.0801920 article EN The Journal of Immunology 2009-03-19

Abstract Introduction Although renal pathology is highly predictive of the disease course in lupus nephritis, it cannot be performed serially because its invasive nature and associated morbidity. The goal this study to investigate whether urinary levels CXC ligand 16 (CXCL16), monocyte chemotactic protein-1 (MCP-1) or vascular cell adhesion molecule-1 (VCAM-1) patients with nephritis are particular features biopsies obtained on day urine procurement. Methods CXCL16, MCP-1, VCAM-1 were...

10.1186/ar3912 article EN cc-by Arthritis Research & Therapy 2012-07-13

Abstract Objective CXCR4 is a chemokine with multiple effects on the immune system. In murine lupus models, we demonstrated that monocytes, neutrophils, and B cells overexpressed its ligand, CXCL12, was up‐regulated in diseased kidneys. We undertook this study to determine whether expression increased peripheral blood leukocytes from patients systemic erythematosus (SLE) CXCL12 kidneys SLE. Methods Peripheral 31 SLE patients, 8 normal controls, 9 rheumatoid arthritis were prospectively...

10.1002/art.27685 article EN Arthritis & Rheumatism 2010-08-19

Abstract The genetic basis of immune-mediated nephritis is poorly understood. Recent studies have demonstrated that the NZW mouse strain more prone to compared with C57BL/6 and BALB/c strains. present study extends these findings by challenging 12 additional inbred strains mice rabbit anti-mouse glomerular basement membrane (GBM) reactive sera. Compared control sera-injected anti-GBM-injected A/J, AKR/J, C3H/HeJ, DBA/2J, MRL/MpJ, NOD/LtJ, P/J, SJL/J, SWR/J mice, BUB/BnJ, DBA/1J, 129/svJ...

10.4049/jimmunol.172.8.5047 article EN The Journal of Immunology 2004-04-15

Crescentic glomerulonephritis (GN) is the most severe form of GN and associated with significant morbidity mortality despite aggressive immunotherapy steroids, cytotoxic drugs, plasmapheresis. We examined therapeutic efficacy green tea polyphenol (−)-epigallocatechin-3-gallate (EGCG, 50 mg/kg BW/day x3weeks), a potent anti-inflammatory anti-oxidant agent, on experimental crescentic induced in 129/svJ mice by administration rabbit anti-mouse glomerular basement membrane sera. Routine...

10.1371/journal.pone.0119543 article EN cc-by PLoS ONE 2015-03-18

Abstract An NZM2410-derived lupus susceptibility locus on murine chromosome 4, Sle2z, has previously been noted to engender generalized B cell hyperactivity. To study how Sle2z impacts tolerance, two Ig H chain site-directed transgenes, 3H9 and 56R, with specificity for DNA were backcrossed onto the C57BL/6 background or without Sle2z. Interestingly, presence of NZM2410 “z” allele Sle2 profoundly breached tolerance DNA, apparently by thwarting receptor editing. Whereas mAbs isolated from...

10.4049/jimmunol.179.2.1340 article EN The Journal of Immunology 2007-07-15

The protective effect of isorhamnetin on myocardial injury induced by isoproterenol (ISO) was investigated to identify key targets and pathways involved, offering potential therapeutic insights for cardiovascular diseases. model established through intraperitoneal ISO injection, the effects apoptosis oxidative stress in ISO-induced rats were assessed. Additionally, an H9c2 cell evaluate impact cellular damage. Transcriptomic sequencing cells conducted differentially expressed genes, followed...

10.20944/preprints202504.0915.v1 preprint EN 2025-04-10

Abstract Objective Although the NZW mouse strain is phenotypically normal, fulminant lupus glomerulonephritis (GN) develops when mice are bred to several other strains, such as NZB, BXSB, B6.Sle1, and B6.Yaa. Based on observation that aging exhibit histologic evidence of GN, we sought test our hypothesis may be more susceptible immune‐mediated renal damage. Methods mice, well C57BL/6 (B6) BALB/c control were challenged with rabbit anti–glomerular basement membrane nephrotoxic sera (NTS),...

10.1002/art.10887 article EN Arthritis & Rheumatism 2003-04-01

Two outstanding questions concerning antinuclear antibodies (ANAs) in lupus involve their pathogenic potential and molecular signatures. To address these questions, a panel of 56 47 nonnuclear binding monoclonal was rescued from four seropositive NZM2410 mice. The monoclonals varied reactivity to nucleosomes, ssDNA, dsDNA, glomerular substrate. A large fraction the demonstrated apparent polyreactivity (to DNA, histones, antigens) due bound, DNase-1 sensitive nuclear antigenic bridges....

10.1084/jem.20030132 article EN The Journal of Experimental Medicine 2004-02-02

Background Mandibuloacral dysplasia (MAD) is a rare autosomal recessive disorder characterized by skeletal abnormalities such as hypoplasia of the mandible and clavicles acro-osteolysis. Other features include cutaneous atrophy lipodystrophy. Two genetic loci are known for MAD: lamin A/C ( LMNA), encoding structural nuclear lamina proteins, zinc metalloproteinase ZMPSTE24), membrane-bound endoprotease involved in post-translational proteolytic cleavage carboxy terminal residues prelamin A to...

10.2310/6650.2006.05068 article EN Journal of Investigative Medicine 2006-05-01

Exercise has been shown to promote wound healing, including tendon repair. Myokines released from the exercised muscles are believed play a significant role in this process. In our previous study, we used an vitro coculture and loading model demonstrate that 2% static of myoblasts increased migration proliferation cocultured tenocytes─two crucial aspects healing. IGF-1, response loading, was identified as contributor proliferation. However, factors responsible for enhanced remained unknown....

10.1021/acs.jproteome.5c00068 article EN cc-by Journal of Proteome Research 2025-04-09

Induction of chronic oxidative stress by glutathione (GSH) depletion has been shown to cause hypertension in normal rats. This was accompanied and perhaps part due inactivation sequestration NO reactive oxygen species (ROS), leading diminished bioavailability. study designed examine renal histology, nitric oxide synthase (NOS) isotype expression, nitrotyrosine distribution this model. Sprague-Dawley rats were subjected administration the GSH inhibitor buthionine sulfoximine (BSO; 30 mM/l...

10.1124/jpet.300.3.762 article EN Journal of Pharmacology and Experimental Therapeutics 2002-03-01

Abstract Innate stimuli are well recognized as adjuvants of the systemic immune response. However, their role in driving end-organ disease is less understood. Whereas passive transfer glomerular-targeting Abs alone elicited minimal renal disease, concomitant delivery innate triggered severe nephritis, characterized by proliferative glomerulonephritis with crescent formation, and tubulointerstitial disease. Specifically, stimulating TLR2, TLR3, TLR4, TLR5 using peptidoglycan, poly(I:C), LPS,...

10.4049/jimmunol.176.1.632 article EN The Journal of Immunology 2006-01-01
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