scholarly journals Sphingolipid-Cholesterol Domains (Lipid Rafts) in Normal Human and Dog Thyroid Follicular Cells Are Not Involved in Thyrotropin Receptor Signaling

Endocrinology ◽  
2004 ◽  
Vol 145 (3) ◽  
pp. 1464-1472 ◽  
Author(s):  
M. J. Costa ◽  
Y. Song ◽  
P. Macours ◽  
C. Massart ◽  
M. C. Many ◽  
...  
Keyword(s):  
Primary Cultures ◽  
Tsh Receptor ◽  
Human Thyroid ◽  
Membrane Domains ◽  
Follicular Cells ◽  
Thyroid Cells ◽  
Caveolin 1 ◽  
Thyroid Follicular Cells ◽  
First Time ◽  
Camp Cascade

Abstract Partition of signaling molecules in sphingolipid-cholesterol-enriched membrane domains, among which are the caveolae, may contribute to signal transduction efficiency. In normal thyroid, nothing is known about a putative TSH/cAMP cascade compartmentation in caveolae or other sphingolipid-cholesterol-enriched membrane domains. In this study we show for the first time that caveolae are present in the apical membrane of dog and human thyrocytes: caveolin-1 mRNA presence is demonstrated by Northern blotting in primary cultures and that of the caveolin-1 protein by immunohistochemistry performed on human thyroid tissue. The TSH receptor located in the basal membrane can therefore not be located in caveolae. We demonstrate for the first time by biochemical methods the existence of sphingolipid-cholesterol-enriched domains in human and dog thyroid follicular cells that contain caveolin, flotillin-2, and the insulin receptor. We assessed a possible sphingolipid-cholesterol-enriched domains compartmentation of the TSH receptor and the α- subunit of the heterotrimeric Gs and Gq proteins using two approaches: Western blotting on detergent-resistant membranes isolated from thyrocytes in primary cultures and the influence of 10 mm methyl-β-cyclodextrin, a cholesterol chelator, on basal and stimulated cAMP accumulation in intact thyrocytes. The results from both types of experiments strongly suggest that the TSH/cAMP cascade in thyroid cells is not associated with sphingolipid-cholesterol-enriched membrane domains.

scholarly journals Detection of SARS-COV-2 receptor ACE-2 mRNA in thyroid cells: a clue for COVID-19-related subacute thyroiditis

2020 ◽  
Author(s):  
M. Rotondi ◽  
F. Coperchini ◽  
G. Ricci ◽  
M. Denegri ◽  
L. Croce ◽  
...  
Keyword(s):  
Primary Cultures ◽  
Thyroid Tissue ◽  
Subacute Thyroiditis ◽  
Human Thyroid ◽  
Thyroid Cell ◽  
Type I ◽  
Rt Pcr ◽  
Follicular Cells ◽  
Thyroid Cells ◽  
Tissue Samples

Abstract Purpose SARS-COV-2 is a pathogenic agent belonging to the coronavirus family, responsible for the current global world pandemic. Angiotensin-converting enzyme 2 (ACE-2) is the receptor for cellular entry of SARS-CoV-2. ACE-2 is a type I transmembrane metallo-carboxypeptidase involved in the Renin-Angiotensin pathway. By analyzing two independent databases, ACE-2 was identified in several human tissues including the thyroid. Although some cases of COVID-19-related subacute thyroiditis were recently described, direct proof for the expression of the ACE-2 mRNA in thyroid cells is still lacking. Aim of the present study was to investigate by RT-PCR whether the mRNA encoding for ACE-2 is present in human thyroid cells. Methods RT-PCR was performed on in vitro ex vivo study on thyroid tissue samples (15 patients undergoing thyroidectomy for benign thyroid nodules) and primary thyroid cell cultures. Results The ACE-2 mRNA was detected in all surgical thyroid tissue samples (n = 15). Compared with two reporter genes (GAPDH: 0.052 ± 0.0026 Cycles−1; β-actin: 0.044 ± 0.0025 Cycles−1; ACE-2: 0.035 ± 0.0024 Cycles−1), the mean level of transcript expression for ACE-2 mRNA was abundant. The expression of ACE-2 mRNA in follicular cells was confirmed by analyzing primary cultures of thyroid cells, which expressed the ACE-2 mRNA at levels similar to tissues. Conclusions The results of the present study demonstrate that the mRNA encoding for the ACE-2 receptor is expressed in thyroid follicular cells, making them a potential target for SARS-COV-2 entry. Future clinical studies in patients with COVID-19 will be required for increase our understanding of the thyroid repercussions of SARS-CoV-2 infection.

Expression of an intercellular adhesion molecule, ICAM-1, by human thyroid cells

1989 ◽  
Vol 122 (1) ◽  
pp. 185-NP ◽  
Author(s):  
A. P. Weetman ◽  
S. Cohen ◽  
M. W. Makgoba ◽  
L. K. Borysiewicz
Keyword(s):  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Human Thyroid ◽  
Accessory Cell ◽  
Graves Disease ◽  
Follicular Cells ◽  
Thyroid Cells ◽  
Hla Dr ◽  
Thyroid Follicular Cells

ABSTRACT Intercellular adhesion molecule-1 (ICAM-1), hitherto identified on activated B cells, macrophages, dendritic cells, endothelia and certain epithelial cells, serves as a ligand for the lymphocyte function-associated antigen-1 (LFA-1). ICAM-1 binding by LFA-1 enhances the efficiency of lymphocyte-target cell and lymphocyte-accessory cell interactions. We have investigated the in-vitro expression of ICAM-1 by cultured thyroid cells from five patients with Graves' disease using indirect immunofluorescence analysis, and found that 30 ± 11% (mean ± s.d.) of cells were ICAM-1 positive under basal conditions. The proportion of cells which were ICAM-1 positive and the amount of ICAM-1 per cell (assessed by fluorescence intensity) were both increased in all cases by the cytokines γ-interferon, interleukin-1 and tumour necrosis factor. Immunohistochemical analysis of frozen sections from thyroidectomy specimens demonstrated ICAM-1 on thyroid follicular cells in areas of lymphocytic infiltration in patients with Graves' disease (n = 2) or Hashimoto's thyroiditis (n = 2). ICAM-1 was not found in specimens from a patient with a toxic multinodular goitre or a patient with Graves' disease without focal lymphocytic accumulation. These results suggest that the thyroid epithelium may express ICAM-1 as well as major histocompatibility complex class II antigens, such as HLA-DR, in response to locally synthesized cytokines. The enhanced expression of ICAM-1 may render these cells more susceptible as targets for lymphocytemediated cytotoxicity, and together with HLA-DR antigen expression may increase the accessory cell capability of the thyroid follicular cells. Journal of Endocrinology (1989) 122, 185–191

Expression of nitric oxide synthase III in human thyroid follicular cells: evidence for increased expression in hyperthyroidism

1997 ◽  
Vol 136 (6) ◽  
pp. 649-655 ◽  
Author(s):  
Ides M Colin ◽  
Peter Kopp ◽  
Jakob Zbären ◽  
André Häberli ◽  
William E Grizzle ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Thyroid Gland ◽  
Tsh Receptor ◽  
Human Thyroid ◽  
Graves Disease ◽  
Follicular Cells ◽  
Thyroid Follicular Cells ◽  
Hypothyroid Patients ◽  
Hyperthyroid Patients

Abstract Nitric oxide mediates a wide array of cellular functions in many tissues. It is generated by three known isoforms of nitric oxide synthases (NOS). Recently, the endothelial isoform, NOSIII, was shown to be abundantly expressed in the rat thyroid gland and its expression increased in goitrous glands. In this study, we analyzed whether NOSIII is expressed in human thyroid tissue and whether levels of expression vary in different states of thyroid gland function. Semiquantitative RT-PCR was used to assess variations in NOSIII gene expression in seven patients with Graves' disease, one with a TSH-receptor germline mutation and six hypothyroid patients (Hashimoto's thyroiditis). Protein expression and subcellular localization were determined by immunohistochemistry (two normal thyroids, five multinodular goiters, ten hyperthyroid patients and two hypothyroid patients). NOSIII mRNA was detected in all samples: the levels were significantly higher in tissues from hyperthyroid patients compared with euthyroid and hypothyroid patients. NOSIII immunoreactivity was detected in vascular endothelial cells, but was also found in thyroid follicular cells. In patients with Graves' disease, the immunostaining was diffusely enhanced in all follicular cells. A more intense signal was observed in toxic adenomas and in samples obtained from a patient with severe hyperthyroidism due to an activating mutation in the TSH receptor. In multinodular goiters, large follicles displayed a weak signal whereas small proliferative follicles showed intense immunoreactivity near the apical plasma membrane. In hypothyroid patients, NOSIII immunoreactivity was barely detectable. In summary, NOSIII is expressed both in endothelial cells and thyroid follicular cells. The endothelial localization of NOSIII is consistent with a role for nitric oxide in the vascular control of the thyroid. NOSIII expression in thyroid follicular cells and the variations in its immunoreactivity suggest a possible role for nitric oxide in thyrocyte function and/or growth. European Journal of Endocrinology 136 649–655

Inhibitory effect of dihydrotestosterone on human thyroid cell growth

1996 ◽  
Vol 151 (2) ◽  
pp. 185-194 ◽  
Author(s):  
R Rossi ◽  
M C Zatelli ◽  
P Franceschetti ◽  
I Maestri ◽  
E Magri ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Primary Cultures ◽  
Inhibitory Effect ◽  
Human Thyroid ◽  
Growth Fraction ◽  
Thyroid Cell ◽  
Mrna Levels ◽  
Follicular Cells ◽  
Thyroid Follicular Cells

Abstract Sex steroid-binding activities have been identified by several authors in normal and pathological thyroids and the expression of the canonic androgen receptor (AR) has recently been demonstrated in human thyroid follicular cells. In order to assess what influence, if any, androgen exposure has on thyroid cell growth, the effect of dihydrotestosterone (DHT) on [3H]thymidine (thy) incorporation and cell proliferation was investigated in thyroid follicular cells in vitro. In a primary culture of goitrous cells, DHT induced a significant reduction of [3H]thy incorporation at concentrations ranging from 10−12 to 10−8 m, with a more pronounced effect at 10−9 m. At this concentration, the inhibitory effect was evident after both 24 and 48 h of treatment and in various types of primary thyroid cell cultures. In goitrous cells, the DHT-induced decrease of [3H]thy was associated with a reduction of expression of the proliferation-associated nuclear Ki-67 antigen, a protein commonly used to assess cell growth fraction. In TPC cells, an AR-positive thyroid papillary carcinoma cell line, DHT at concentrations between 10−12 and 10−8 m significantly decreased the growth rate. DHT (10−9 m) produced an approximately 50–60% inhibition of cell proliferation and the antiandrogen cyproterone acetate was capable of reversing such effects. The DHT-induced reduction of TPC cell proliferation was associated with a significant reduction of c-myc RNA levels. Thyroperoxidase mRNA levels and thyroglobulin production were not reduced by androgen in primary cultures of goitrous cells. In conclusion, our results indicated that androgens may have a role in this gland by reducing the proliferation, but not the function, of follicular cells. Journal of Endocrinology (1996) 151, 185–194

scholarly journals An Amphotropic Retroviral Vector Expressing a Mutant gsp Oncogene: Effects on Human Thyroid Cells in Vitro1

1997 ◽  
Vol 82 (8) ◽  
pp. 2702-2709 ◽  
Author(s):  
M. Ivan ◽  
M. Ludgate ◽  
V. Gire ◽  
J. A. Bond ◽  
D. Wynford-Thomas
Keyword(s):  
Retroviral Vector ◽  
Human Thyroid ◽  
Nodule Formation ◽  
Target Cells ◽  
Follicular Cells ◽  
Morphological Response ◽  
Thyroid Cells ◽  
Significant Difference ◽  
Thyroid Follicular Cells ◽  
Normal Human

Point mutations of the gsp protooncogene (encoding theα -subunit of the Gs protein) that constitutively activate the cAMP signaling pathway are a common feature of and a plausible causative mechanism for thyroid hyperfunctioning adenomas (hot nodules). To investigate the extent to which mutant gsp acting alone can induce proliferation of thyroid follicular cells, we generated an amphotropic retroviral vector (based on the pBABE-neo plasmid and psi-CRIP packaging line) to permit stable introduction of a hemagglutinin-tagged Gln227→Leu mutant gsp gene into normal human thyrocytes in vitro. The biological activity of the vector was confirmed by detection of HA-tagged Gsp protein expression and induction of cAMP synthesis in selected target cells. Normal human thyroid follicular cells in primary monolayer culture were infected with the gsp retroviral vector or with corresponding vectors expressing mutant H-ras or neo only as positive and negative controls, respectively. Although, as before, mutant ras generated 10–20 well differentiated epithelial colonies/dish of 105 infected cells, with an average lifespan of 15–20 population doublings, only small groups of no more than 15–50 differentiated thyrocytes were observed with the gsp vector. In addition to standard conditions (10% FCS), infections were performed in reduced serum (1% FCS, TSH, and insulin), in the presence of isobutylylmethylxanthine, or in the presence of agents capable of closing gap junctions, with no significant difference in outcome. Although little or no proliferative response was observed regardless of the conditions, there was clear evidence of morphological response (rearrangement of the actin cytoskeleton and increased cell size). The results suggest that gsp mutation may not be a sufficient proliferogenic stimulus by itself to account for hot nodule formation.

scholarly journals Progesterone Upregulates Gene Expression in Normal Human Thyroid Follicular Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Ana Paula Santin Bertoni ◽  
Ilma Simoni Brum ◽  
Ana Caroline Hillebrand ◽  
Tania Weber Furlanetto
Keyword(s):  
Mrna Expression ◽  
Cell Function ◽  
Human Thyroid ◽  
Thyroid Cell ◽  
Sodium Iodide Symporter ◽  
Follicular Cells ◽  
Ki 67 ◽  
Thyroid Cells ◽  
Female Sex Hormones ◽  
Thyroid Follicular Cells

Thyroid cancer and thyroid nodules are more prevalent in women than men, so female sex hormones may have an etiological role in these conditions. There are no data about direct effects of progesterone on thyroid cells, so the aim of the present study was to evaluate progesterone effects in the sodium-iodide symporterNIS, thyroglobulinTG, thyroperoxidaseTPO, andKI-67genes expression, in normal thyroid follicular cells, derived from human tissue.NIS,TG,TPO, andKI-67mRNA expression increased significantly after TSH 20 μUI/mL, respectively: 2.08 times,P<0.0001; 2.39 times,P=0.01; 1.58 times,P=0.0003; and 1.87 times,P<0.0001. In thyroid cells treated with 20 μUI/mL TSH plus 10 nM progesterone, RNA expression ofNIS,TG, andKI-67genes increased, respectively: 1.78 times,P<0.0001; 1.75 times,P=0.037; and 1.95 times,P<0.0001, andTPOmRNA expression also increased, though not significantly (1.77 times,P=0.069). These effects were abolished by mifepristone, an antagonist of progesterone receptor, suggesting that genes involved in thyroid cell function and proliferation are upregulated by progesterone. This work provides evidence that progesterone has a direct effect on thyroid cells, upregulating genes involved in thyroid function and growth.

Studies of catecholamine effect on cyclic AMP in human cultured thyroid cells: their interaction with thyrotrophin receptor

1983 ◽  
Vol 102 (1) ◽  
pp. 62-67 ◽  
Author(s):  
Roberto S. Toccafondi ◽  
Maria Luisa Brandi ◽  
Carlo M. Rotella ◽  
Roberto Zonefrati
Keyword(s):  
Cyclic Amp ◽  
Adrenergic Receptors ◽  
Human Thyroid ◽  
Adrenergic Nerve ◽  
Camp Accumulation ◽  
Follicular Cells ◽  
Functional Responses ◽  
Thyroid Cells ◽  
Thyroid Follicular Cells ◽  
Bovine Tsh

Abstract. Even though adrenergic nerve terminals between and around thyroid follicles and catecholamine stimulation of thyroid adenylate cyclase have been reported, there is no uniform concept on catecholamine interaction with thyrotrophin (TSH) receptors. Therefore, the effect of catecholamines on TSH-stimulated cyclic AMP (cAMP) accumulation in human follicular thyroid cells has been investigated, to thus eliminating the extrathyroidal actions of catecholamines. Epinephrine, norepinephrine and isoproterenol appeared to be rapid and potent stimulators of intracellular cAMP accumulation, the half maximum increase doses being 4 × 10−7m, 1 × 10−5m and 5 × 10−7m, respectively. While propranolol (1 × 10−5m) prevented the stimulatory effect of catecholamines and failed to inhibit the effect of bovine TSH, phentolamine (1 × 10−5m) enhanced the potency of norepinephrine and bovine TSH, leaving that of epinephrine unchanged. The effects of epinephrine (2 × 10−8m) and isoproterenol (2 × 10−8m) were additive to that of bovine TSH (0.5 mU/ml), but the effect of simultaneous stimulation with norepinephrine (5 × 10−7m) and bovine TSH (0.5 mU/ml) was lower than expected. Prenalterol, a selective β1-agonist, did not stimulate cAMP accumulation, while terbutaline, a selective β2-agonist, exerted a potent stimulation. Metoprolol, a selective β1-adrenergic blocker, did not affect the response of thyroid follicular cells to isoproterenol. These results demonstrate the existence of β-adrenergic receptors in human thyroid follicular cells, mainly of the type β2, apparently not correlated with TSH receptor. The existence of α-adrenergic receptors which counter-regulate TSH functional responses in human thyroid follicular cells is suggested.

Monoclonal antibodies to the human TSH receptor: epitope mapping and binding to the native receptor on the basolateral plasma membrane of thyroid follicular cells

1996 ◽  
Vol 16 (2) ◽  
pp. 159-170 ◽  
Author(s):  
L B Nicholson ◽  
H Vlase ◽  
P Graves ◽  
M Nilsson ◽  
J Molne ◽  
...  
Keyword(s):  
Amino Acids ◽  
Monoclonal Antibodies ◽  
Plasma Membrane ◽  
Extracellular Domain ◽  
Tsh Receptor ◽  
Follicular Cells ◽  
Thyroid Cells ◽  
Extracellular Region ◽  
Thyroid Follicular Cells ◽  
Basolateral Plasma Membrane

ABSTRACT We have characterized four murine monoclonal antibodies (mAbs) to the extracellular domain of the human TSH receptor (TSH-R.E), the target autoantigen of Graves' disease. Recombinant TSH-R.E used as immunogen, was produced in E. coli as a fusion protein with glutathione-S-transferase or in a baculovirus-insect cell system, as a non-fusion glycoprotein. To increase the epitope specificity of the mAbs, two different strains of mice (H-2b and H-2d) were immunized. The epitopes recognized by the mAbs were characterized by immunoblotting with various recombinant constructs of TSH-R.E and by binding to overlapping synthetic peptides of the receptor. The four IgG mAbs characterized recognized epitopes localized to different regions on the TSH-R.E; amino acids 22–35 (A10 and All, both IgG2b from H-2b animals), amino acids 402–415 (A7, IgG2b from H-2b animals) and amino acids 147–228 (A9, IgG1 from H-2d animals). Immunolocalization studies showed that mAb A9 recognized TSH-R.E on unfixed cryostat sections, where binding was localized to the basolateral plasma membrane of thyroid follicular cells, suggesting that this antibody reacts with the native receptor on thyroid cells. The binding of the mAbs A7, A10 and All was also restricted to the basal surface of thyroid cells, but only after acetone fixation of the sections, implying that the epitopes recognized on the amino and carboxyl terminus of the extracellular region of the receptor are not accessible on the native molecule. None of the mAbs stimulated cyclic AMP responses in COS-7 cells transiently transfected with full-length functioning TSH-R.E, whilst weak inhibition of binding of radiolabelled TSH to porcine membranes in a radioreceptor assay was apparent with mAb A10 and All, but only at high concentrations of IgG. The ability of mAb A9 to bind to the native receptor without stimulating activity or inhibition of TSH binding suggests that antibody can bind to the central region of the TSH-R.E without perturbing receptor function. The availability of mAbs that recognize epitopes on different regions of the extracellular domain of TSH-R will lead to a better understanding of the autoantigenic regions on TSH-R implicated in disease activity.

Effects of 4,4′-di-isothiocyano-2,2′-stilbene disulphonate on iodide uptake by primary cultures of turtle thyroid follicular cells

1987 ◽  
Vol 113 (3) ◽  
pp. 403-412 ◽  
Author(s):  
S. Y. Chow ◽  
Y. C. Yen-Chow ◽  
H. S. White ◽  
D. M. Woodbury
Keyword(s):  
Cultured Cells ◽  
Primary Cultures ◽  
Thyroid Tissue ◽  
Concentration Addition ◽  
Thyroid Cell ◽  
Follicular Cells ◽  
Iodide Uptake ◽  
Thyroid Cells ◽  
Thyroid Follicular Cells ◽  
Cell Medium

ABSTRACT Iodide uptake by primary cultures of turtle thyroid follicular cells is directly proportional to the Na + concentration and is inversely proportional to the HCO3− concentration in culture medium, but is not affected by the Cl− concentration. Addition of 4,4′-di-isothiocyano-2,2′-stilbene disulphonate (DIDS; 10 μmol/l and higher doses) to medium containing different concentrations of Na+ (5–140 mmol/l), HCO3− (0–40 mmol/l) and Cl − (120 mmol/l) generally enhanced iodide uptake by the cultured cells; however, there was no significant effect in Na+-free and in low Cl− (90 mmol/l and less) medium. The inhibitory effects on iodide uptake of ouabain, frusemide and perchlorate were attenuated by DIDS which also antagonized the stimulatory effects on iodide uptake of TSH, although both DIDS and TSH increased the 125I− cell/medium ratio when they were given alone. At doses of 100 μmol/l and higher, DIDS lowered the intracellular pH of cultured cells when the pH of the medium was maintained at a constant level. It also increased the intracellular Cl − concentration, but had no effect on intracellular Na+ or K +. The input and specific resistances of cell membranes in cultured thyroid cells and in isolated thyroid slices increased (decreased conductance) after adding DIDS to the perfusion fluids. Both Na+/K+- and HCO3−-ATPase activities in homogenates of turtle thyroid tissue were inhibited by DIDS. Results from this investigation demonstrate (1) that in addition to preventing the leak of iodide from thyroid cells, DIDS may act to increase the sensitivity of the Na + -anion carrier to I− and thereby increases iodide uptake, and (2) that a HCO3−–Cl− exchange system is present in the thyroid cell membrane and appears to be linked to the transport of iodide into thyroid cells. J. Endocr. (1987) 113, 403–412

scholarly journals Modulation of ACE-2 mRNA by inflammatory cytokines in human thyroid cells: a pilot study

Endocrine ◽  
2021 ◽  
Author(s):  
Francesca Coperchini ◽  
Gianluca Ricci ◽  
Laura Croce ◽  
Marco Denegri ◽  
Rubina Ruggiero ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Combination Treatment ◽  
Primary Cultures ◽  
Human Thyroid ◽  
Thyroid Cell ◽  
Mrna Levels ◽  
Thyroid Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Pro Inflammatory Cytokines

Abstract Introduction Angiotensin-converting-enzyme-2 (ACE-2) was demonstrated to be the receptor for cellular entry of SARS-CoV-2. ACE-2 mRNA was identified in several human tissues and recently also in thyroid cells in vitro. Purpose Aim of the present study was to investigate the effect of pro-inflammatory cytokines on the ACE-2 mRNA levels in human thyroid cells in primary cultures. Methods Primary thyroid cell cultures were treated with IFN-γ and TNF-α alone or in combination for 24 h. ACE-2 mRNA levels were measured by RT-PCR. As a control, the levels of IFN-γ inducible chemokine (CXCL10) were measured in the respective cell culture supernatants. Results The mean levels of ACE-2 mRNA increased after treatment with IFN-γ and TNF-α in all the thyroid cell preparations, while the combination treatment did not consistently synergically increase ACE-2-mRNA. At difference, CXCL10 was consistently increased by IFN-γ and synergically further increased by the combination treatment with IFN-γ + TNF-α, with respect to IFN-γ alone. Conclusions The results of the present study show that IFN-γ and, to a lesser extent TNF-α consistently increase ACE-2 mRNA levels in NHT primary cultures. More interestingly, the combined stimulation (proven to be effective according to the synergic effect registered for CXCL10) produces different responses in terms of ACE-2 mRNA modulation. These results would suggest that elevated levels of pro-inflammatory cytokines could facilitate the entering of the virus in cells by further increasing ACE-2 expression and/or account for the different degree of severity of SARS-COV-2 infection. This hypothesis deserves to be confirmed by further specific studies.

Sign in / Sign up

Export Citation Format

Share Document