Tie-2 Is Overexpressed by Monocytes in Autoimmune Thyroid Disorders and Participates in Their Recruitment to the Thyroid Gland

Figueroa-Vega, Nicté; Alfonso-Pérez, Manuel; Cuesta-Mateos, Carlos; Sánchez-Madrid, Francisco; Moreno–Otero, Ricardo; González‐Amaro, Roberto; Marazuela, Mónica

doi:10.1210/jc.2009-0220

Cited by 11 publications

(7 citation statements)

References 41 publications

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“…Evidence of the important role of chemokines and integrins has been found previously in AITD in the up-regulation of CCL2 (14) and that of soluble intercellular adhesion molecule-1 (sICAM-1 or soluble cluster of differentiation 54) in the serum of patients (15,16). There are also indications that the angiopoietin-1 receptor (TIE-2) system has a role in the recruitment of monocytes to the thyroid gland in AITD (17).…”

Section: T He Etiology Of Autoimmune Thyroid Disease (Aitd)mentioning

confidence: 83%

Changes in Serum Adhesion Molecules, Chemokines, Cytokines, and Tissue Remodeling Factors in Euthyroid Women Without Thyroid Antibodies Who Are at Risk for Autoimmune Thyroid Disease: A Hypothesis on the Early Phases of the Endocrine Autoimmune Reaction

Beumer

Effraimidis

Drexhage

et al. 2013

The Journal of Clinical Endocrinology &Amp; Metabolism

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Section: T He Etiology Of Autoimmune Thyroid Disease (Aitd)mentioning

confidence: 83%

Changes in Serum Adhesion Molecules, Chemokines, Cytokines, and Tissue Remodeling Factors in Euthyroid Women Without Thyroid Antibodies Who Are at Risk for Autoimmune Thyroid Disease: A Hypothesis on the Early Phases of the Endocrine Autoimmune Reaction

Beumer

Effraimidis

Drexhage

et al. 2013

The Journal of Clinical Endocrinology &Amp; Metabolism

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“…Some top hub genes may also participate in immunomodulation. ANGPT2 can recruit monocytes [57,58], which results in suppressing T cell activation [59]. MPZL2 could regulate the development of the thymus and T cell function [60,61].…”

Section: Discussionmentioning

confidence: 99%

Transcriptome differences in adipose stromal cells derived from pre- and postmenopausal women

et al. 2020

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Background: As the population ages, an increasing number of postmenopausal women are donors of adipose stromal cells (ASCs) and may benefit from autologous ASC-related treatments. However, the effect of menopausal status on ASCs has not been investigated. Methods: RNA sequencing data were downloaded, and differentially expressed genes (DEGs) were identified. Hierarchical clustering, Gene Ontology, and pathway analyses were applied to the DEGs. Two gene coexpression network analysis approaches were applied to the DEGs to provide a holistic view and preserve gene interactions. Hub genes of the gene coexpression network were identified, and their expression profiles were examined with clinical samples. ASCs from pre-and postmenopausal women were co-cultured with monocytes and T cells to determine their immunoregulatory role. Results: In total, 2299 DEGs were identified and presented distinct expression profiles between pre-and postmenopausal women. Gene Ontology and pathway analyses revealed some fertility-, sex hormone-, immune-, aging-, and angiogenesis-related terms and pathways. Gene coexpression networks were constructed, and the top hub genes, including TIE1, ANGPT2, RNASE1, PLVAP, CA2, and MPZL2, were consistent between the two approaches. Expression profiles of hub genes from the RNA sequencing data and clinical samples were consistent. ASCs from postmenopausal women elicit M1 polarization, while their counterparts facilitate CD3/4+ T cell proliferation. Conclusions: The present study reveals the transcriptome differences in ASCs derived from pre-and postmenopausal women and provides holistic views by preserving gene interactions via gene coexpression network analysis. The top hub genes identified by this study could serve as potential targets to enhance the therapeutic potential of ASCs.

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“…For example, T cells show higher production of IFN-γ, IL-1 and TNF-α, which potentiates the expression of adhesion molecule receptors thereby augmenting autoimmune response (41). Interestingly, AITD associated rise in the vasculature of the intra-thyroid environment is in coherence with the high concentrations of vascular endothelial growth factor (VEGF), angiopoietins (Ang-1 and Ang-2) and tyrosine kinase receptor Tie-2 family signaling molecules (important for angiogenesis and vascularization) (42). There are reports of monocytes expressing Tie-2 that are recruited to inflammation foci or neoplastic center (43).…”

Section: Molecules Participating In the Destruction Of Thyroidmentioning

confidence: 99%

“…There are reports of monocytes expressing Tie-2 that are recruited to inflammation foci or neoplastic center (43). All these events compound up in causing tissue damage evident in AITD (42).…”

Section: Molecules Participating In the Destruction Of Thyroidmentioning

confidence: 99%

Molecular Insights Into the Relationship Between Autoimmune Thyroid Diseases and Breast Cancer: A Critical Perspective on Autoimmunity and ER Stress

et al. 2019

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The etiopathologies behind autoimmune thyroid diseases (AITDs) unravel misbehavior of immune components leading to the corruption of immune homeostasis where thyroid autoantigens turn foe to the self. In AITDs lymphocytic infiltration in the thyroid shows up a deranged immune system charging the follicular cells of the thyroid gland (thyrocytes) leading to the condition of either hyperthyroidism or hypothyroidism. The inflammation in AITDs consistently associate with ER function due to which disturbances in the ER protein homeostasis leads to unfolded protein response (UPR) that promotes pathogenesis of autoimmunity. The roles of ER stress in the instantaneous downregulation of MHC class I molecules on thyrocytes and the relevance of IFN γ in the pathogenesis of AITD has been well-documented. Thyroglobulin being the major target of autoantibodies in most of the AITDs is because of its unusual processing in the ER. Autoimmune disorders display a conglomeration of ER stress-induced UPR activated molecules. Several epidemiological data highlight the preponderance of AITDs in women as well as its concurrence with breast cancer. Both being an active glandular system displaying endocrine activity, thyroid as well as breast tissue show various commonalities in the expression pattern of heterogenous molecules that not only participate in the normal functioning but at the same time share the blame during disease establishment. Studies on the development and progression of breast carcinoma display a deranged and uncontrolled immune response, which is meticulously exploited during tumor metastasis. The molecular crosstalks between AITDs and breast tumor microenvironment rely on active participation of immune cells. The induction of ER stress by Tunicamycin advocates to provide a model for cancer therapy by intervening glycosylation. Therefore, this review attempts to showcase the molecules that are involved in feeding up the relationship between breast carcinoma and AITDs.

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Tie-2 Is Overexpressed by Monocytes in Autoimmune Thyroid Disorders and Participates in Their Recruitment to the Thyroid Gland

Abstract: Our data suggest that the Ang/Tie-2 system, through the participation of blood vessels, inflammatory cells, and TFC, may have an important role in the recruitment of monocytes to the thyroid gland and the pathogenesis of the tissue damage seen in AITD.

Cited by 11 publications

References 41 publications

Changes in Serum Adhesion Molecules, Chemokines, Cytokines, and Tissue Remodeling Factors in Euthyroid Women Without Thyroid Antibodies Who Are at Risk for Autoimmune Thyroid Disease: A Hypothesis on the Early Phases of the Endocrine Autoimmune Reaction

Changes in Serum Adhesion Molecules, Chemokines, Cytokines, and Tissue Remodeling Factors in Euthyroid Women Without Thyroid Antibodies Who Are at Risk for Autoimmune Thyroid Disease: A Hypothesis on the Early Phases of the Endocrine Autoimmune Reaction

Transcriptome differences in adipose stromal cells derived from pre- and postmenopausal women

Molecular Insights Into the Relationship Between Autoimmune Thyroid Diseases and Breast Cancer: A Critical Perspective on Autoimmunity and ER Stress

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