Редактирование: CCL17 (раздел)

==Publications==

{{medline-entry
|title=Aging and chronic high-fat feeding negatively affects kidney size, function, and gene expression in CTRP1-deficient mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33085906
|abstract=C1q/TNF-related protein 1 (CTRP1) is an endocrine factor with metabolic, cardiovascular, and renal functions. We previously showed that aged Ctrp1 knockout (KO) mice fed a control low-fat diet develop renal hypertrophy and dysfunction. Since aging and obesity adversely affects various organ systems, we hypothesized that aging, in combination with obesity induced by chronic high-fat feeding, would further exacerbates renal dysfunction in CTRP1-deficient animals. To test this, we fed wild-type and Ctrp1 KO mice a high-fat diet for eight months or longer. Contrary to our expectation, no differences were observed in blood pressure, heart function, or vascular stiffness between genotypes. Loss of CTRP1, however, resulted in ~2-fold renal enlargement (relative to body weight), ~60% increase in urinary total protein content and elevated pH, and changes in renal gene expression affecting metabolism, signaling, transcription, cell adhesion, solute and metabolite transport, and inflammation. Assessment of glomerular integrity, the extent of podocyte foot process effacement, as well as renal response to water restriction and salt loading did not reveal significant differences between genotypes. Interestingly, blood platelet, white blood cell, neutrophil, lymphocyte, and eosinophil counts were significantly elevated, whereas mean corpuscular volume and hemoglobin were reduced in Ctrp1-KO mice. Cytokine profiling revealed increased circulating levels of [[CCL17]] and TIMP-1 in KO mice. Compared to our previous study, current data suggest that chronic high-fat feeding affects renal phenotypes differently than similarly aged mice fed a control low-fat diet, highlighting a diet-dependent contribution of CTRP1 deficiency to age-related changes in renal structure and function.

|keywords=* aging
* heart
* kidney
* metabolism
* obesity
|full-text-url=https://sci-hub.do/10.1152/ajpregu.00139.2020
}}
{{medline-entry
|title=Senescent thyrocytes and thyroid tumor cells induce M2-like macrophage polarization of human monocytes via a PGE2-dependent mechanism.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31113465
|abstract=Thyroid carcinoma includes several variants characterized by different biological and clinical features: from indolent microcarcinoma to undifferentiated and aggressive anaplastic carcinoma. Inflammation plays a critical role in thyroid tumors. Conditions predisposing to cancer, as well as oncogene activity, contribute to the construction of an inflammatory microenvironment that facilitates thyroid tumor progression. Moreover, oncogene-induced senescence, a mechanism tightly connected with inflammation, and able to restrain or promote cancer progression, is involved in thyroid cancer. The interactions between thyroid tumor cells and the microenvironment are not completely clarified. We characterize in vitro the interplay between macrophages and senescent thyrocytes and tumor-derived cell lines, modeling early and late thyroid tumor stages, respectively. Purified peripheral blood-derived human monocytes were exposed to thyroid cell-derived conditioned medium (CM) and assessed for phenotype by flow cytometry. The factors secreted by thyroid cells and macrophages were identified by gene expression analysis and ELISA. The protumoral effect of macrophages was assessed by wound healing assay on K1 thyroid tumor cells. The expression of [[PTGS2]] and M2 markers in thyroid tumors was investigated in publicly available datasets. Human monocytes exposed to CM from senescent thyrocytes and thyroid tumor cell lines undergo M2-like polarization, showing high CD206 and low MHC II markers, and upregulation of [[CCL17]] secretion. The obtained M2-like macrophages displayed tumor-promoting activity. Among genes overexpressed in polarizing cells, we identified the prostaglandin-endoperoxide synthase enzyme ([[PTGS2]]/COX-2), which is involved in the production of prostaglandin E2 (PGE2). By using COX-2 inhibitors we demonstrated that the M2-like polarization ability of thyroid cells is related to the production of PGE2. Co-expression of [[PTGS2]] and M2 markers is observed a significant fraction of human thyroid tumors. Our results demonstrate that both senescent thyrocytes and thyroid tumor cell lines trigger M2-like macrophage polarization that is related to PGE2 secretion. This suggests that the interaction with the microenvironment occurs at both early and late thyroid tumor stages, and favors tumor progression. The co-expression of [[PTGS2]] gene and M2 markers in human thyroid carcinoma highlights the possibility to counteract tumor growth through COX-2 inhibition.
|mesh-terms=* Cell Differentiation
* Cell Line, Tumor
* Cell Polarity
* Cellular Senescence
* Chemokine CCL17
* Culture Media, Conditioned
* Cyclooxygenase 2
* Cyclooxygenase 2 Inhibitors
* Flow Cytometry
* Gene Expression Regulation, Neoplastic
* Humans
* Inflammation
* Macrophages
* Monocytes
* Signal Transduction
* Thyroid Epithelial Cells
* Thyroid Gland
* Thyroid Neoplasms
|keywords=* COX-2
* HRAS
* Macrophages
* Oncogene-induced senescence
* PGE2
* Thyrocytes
* Thyroid carcinoma
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6528237
}}