Publications by authors named "Marcelo-Heron Petri"

5 Publications

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Osteopontin: another piece in the systemic lupus erythematosus immunopathology puzzle.

Clin Exp Rheumatol 2021 May 5. Epub 2021 May 5.

Universidad de Guadalajara, Centro Universitario de Ciencias de la Salud, Departamento de Biología Molecular y Genómica, Instituto de Investigación en Reumatología y del Sistema Músculo Esquelético (IIRSME), Guadalajara; UDG-CA-703, Inmunología y Reumatología, Guadalajara, and Hospital Civil de Guadalajara Dr Juan I. Menchaca, División de Medicina Interna, Servicio de Reumatología, CONACyT PNPC, Guadalajara, Mexico.

Osteopontin (OPN) is a phosphoglycoprotein involved in bone remodelling, wound healing, cell adhesion, tissue remodelling, and immune response that is distributed widely in normal adult tissues. OPN biological activity is regulated by thrombin and matrix metalloproteinases (MMPs) cleavage, where the full-length (OPN-FL) protein and the cleaved OPN-N are associated with autoimmune diseases such as systemic lupus erythematosus (SLE). OPN overexpression has been associated with a predisposition to SLE and bad prognosis since OPN could mediate a sustained polyclonal B cell activation that besides to intracellular OPN (iOPN) form, promote the T follicular helper (TFH) cells and enhance anti-nuclear antibody production. Currently, the role of OPN in lupus nephritis (LN) has been reported and extensively studied; however, no data are available about the potential mechanism of OPN in neuropsychiatric SLE (NPSLE). In this review, we highlighted the contribution of OPN and iOPN in LN and NPSLE immunopathology.
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May 2021

Inverse Relationship of the CMKLR1 Relative Expression and Chemerin Serum Levels in Obesity with Dysmetabolic Phenotype and Insulin Resistance.

Mediators Inflamm 2016 28;2016:3085390. Epub 2016 Apr 28.

Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Sierra Mojada No. 950 Colonia Independencia, CP 44340, Guadalajara, JAL, Mexico; Instituto de Investigación en Reumatología y del Sistema Musculo Esquelético, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Sierra Mojada No. 950 Colonia Independencia, CP 44340, Guadalajara, JAL, Mexico; UDG-CA-703, Grupo de Investigación en Inmunología y Reumatología, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Sierra Mojada No. 950 Colonia Independencia, CP 44340, Guadalajara, JAL, Mexico; Servicio de Reumatología, División de Medicina Interna, Hospital Civil "Dr. Juan I. Menchaca", Universidad de Guadalajara, Salvador de Quevedo y Zubieta No. 750, CP 44340, Guadalajara, JAL, Mexico.

Background: In obesity there is a subclinical chronic low-grade inflammatory response where insulin resistance (IR) may develop. Chemerin is secreted in white adipose tissue and promotes low-grade inflammatory process, where it expressed CMKLR1 receptor. The role of chemerin and CMKLR1 in inflammatory process secondary to obesity is not defined yet.

Methods: Cross-sectional study with 134 individuals classified as with and without obesity by body mass index (BMI) and IR. Body fat storage measurements and metabolic and inflammatory markers were measured by routine methods. Soluble chemerin and basal levels of insulin by ELISA and relative expression of CMKLR1 were evaluated with qPCR and 2(-ΔΔCT) method.

Results: Differences (P < 0.05) were observed between obesity and lean individuals in body fat storage measurements and metabolic-inflammatory markers. Both CMKLR1 expression and chemerin levels were increased in obesity without IR. Soluble chemerin levels correlate with adiposity and metabolic markers (r = 8.8% to 38.5%), P < 0.05.

Conclusion: The increment of CMKLR1 expression was associated with insulin production. Increased serum levels of chemerin in obesity were observed, favoring a dysmetabolic response. The results observed in this study suggest that both chemerin and CMKLR1 have opposite expression in the context of low-grade inflammatory response manifested in the development of IR.
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http://dx.doi.org/10.1155/2016/3085390DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4864190PMC
January 2017

CCL2 Serum Levels and Adiposity Are Associated with the Polymorphic Phenotypes -2518A on CCL2 and 64ILE on CCR2 in a Mexican Population with Insulin Resistance.

J Diabetes Res 2016 29;2016:5675739. Epub 2015 Dec 29.

Instituto de Investigación en Reumatología y del Sistema Musculo Esquelético, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Sierra Mojada No. 950, Colonia Independencia, 44340 Guadalajara, JAL, Mexico; UDG-CA-701, Grupo de Investigación Inmunometabolismo en Enfermedades Emergentes (GIIEE), Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Sierra Mojada No. 950, Colonia Independencia, 44340 Guadalajara, JAL, Mexico; Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Sierra Mojada No. 950, Colonia Independencia, 44340 Guadalajara, JAL, Mexico; Departamento de Farmacobiología, Centro Universitario de Ciencias Exactas e Ingenierías, Universidad de Guadalajara, Boulevard Marcelino García Barragán No. 1421, 44430 Guadalajara, JAL, Mexico.

Genetic susceptibility has been described in insulin resistance (IR). Chemokine (C-C motif) ligand-2 (CCL2) is overexpressed in white adipose tissue and is the ligand of C-C motif receptor-2 (CCR2). The CCL2 G-2518A polymorphism is known to regulate gene expression, whereas the physiological effects of the CCR2Val64Ile polymorphism are unknown. The aim of the study is to investigate the relationship between these polymorphisms with soluble CCL2 levels (sCCL2), metabolic markers, and adiposity. In a cross-sectional study we included 380 Mexican-Mestizo individuals, classified with IR according to Stern criteria. Polymorphism was identified using PCR-RFLP/sequence-specific primers. Anthropometrics and metabolic markers were measured by routine methods and adipokines and sCCL2 by ELISA. The CCL2 polymorphism was associated with IR (polymorphic A+ phenotype frequencies were 70.9%, 82.6%, in individuals with and without IR, resp.). Phenotype carriers CCL2 (A+) displayed lower body mass and fat indexes, insulin and HOMA-IR, and higher adiponectin levels. Individuals with IR presented higher sCCL2 compared to individuals without IR and was associated with CCR2 (Ile+) phenotype. The double-polymorphic phenotype carriers (A+/Ile+) exhibited higher sCCL2 than double-wild-type phenotype carriers (A-/Ile-). The present findings suggest that sCCL2 production possibly will be associated with the adiposity and polymorphic phenotypes of CCL2 and CCR2, in Mexican-Mestizos with IR.
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http://dx.doi.org/10.1155/2016/5675739DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4709622PMC
December 2016

Differential regulation of monocytic expression of leukotriene and lipoxin receptors.

Prostaglandins Other Lipid Mediat 2015 Sep 3;121(Pt A):138-43. Epub 2015 Aug 3.

Department of Medicine, Karolinska Institutet and Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.

Introduction: Lipoxygenase pathway yields both pro-inflammatory leukotrienes and pro-resolving lipoxins. The aim of the present study was to determine the effects of T-lymphocytes and pro-inflammatory stimuli on the expression levels of the lipoxin FPR2/ALX receptor, and the leukotriene BLT1 receptor in monocytes and macrophages, and to characterize LXA4-induced effects on pro-inflammatory mediators.

Methods: Human macrophages were co-cultured with activated CD4(+) cells. THP-1 cells were stimulated with different cytokines, LXA4 and supernatant from activated CD4(+) cells. mRNA was extracted for qPCR experiments and protein was analyzed by flow cytometry.

Results: Co-culture of macrophages with activated CD4(+) cells or their supernatants up-regulated macrophage FPR2/ALX expression but did not alter BLT1 receptor expression. Monocyte stimulation with IFN-γ up-regulated FPR2/ALX mRNA and protein levels, whereas BLT1 mRNA was down-regulated. Finally, LXA4 decreased mRNA levels of MMP-9, CXCL16, IL-1β, and IL-8 in THP-1 cells.

Conclusion: The present study shows that pro-inflammatory stimuli lead to FPR2/ALX expression. LXA4 induces an anti-inflammatory response, which could participate in the resolution of inflammation.
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http://dx.doi.org/10.1016/j.prostaglandins.2015.07.005DOI Listing
September 2015

[Histological and molecular alterations in inflammatory myopathies].

Reumatol Clin 2009 Nov 30;5 Suppl 3:20-2. Epub 2009 Oct 30.

Instituto de Investigación en Reumatología y del Sistema Músculo Esquelético, CUCS, Universidad de Guadalajara, Jalisco, México.

The histological findings in muscle biopsies of inflammatory myopathies have been divided into 2 groups: A) Endomisial infiltrates mainly by T CD8+, CD4+ and macrophages and B) Perivascular infiltrates by CD4+, B cells and macrophages. The first kind of infiltrate suggests an immune reaction against muscle fibers very common in PM and inclusion body myositis, On the other hand the perivascular infiltrate is a hallmark of DM. It has ben shown that autoantigens related with myopathies such as Mi-2, Jo-1, OJ, PL12, Ku, PM/Scl are able to suffer proteolytic cleavage by granzyme B and other stimulus induced by cytotoxic T cells. In this chapter we will review the histological and molecular findings of inflammatory myopathies but we will also discuss a special group of myopathies related to the presence of antibodies against the SRP complex, in particular the SRP72 and SRP54 antibodies, which are associated with a poor prognosis and clinical outcome and present an inadequate response to conventional treatment.
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http://dx.doi.org/10.1016/j.reuma.2009.07.007DOI Listing
November 2009