scholarly journals Immunohistochemistry for (Pro)renin Receptor in Humans

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Satoshi Morimoto ◽  
Noriko Morishima ◽  
Daisuke Watanabe ◽  
Yoichiro Kato ◽  
Noriyuki Shibata ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Protein Expression ◽  
Expression Pattern ◽  
Receptor Expression ◽  
Whole Body ◽  
Receptor Protein ◽  
Pituitary Hormone ◽  
Human Organ ◽  
Human Organs ◽  
Almost All

The (pro)renin receptor is a multifunctional protein with roles in angiotensin-II-dependent and -independent intracellular cell signaling and roles as an intracellular accessory protein for the vacuolar H+-ATPase, including hormone secretion. While (pro)renin receptor mRNA is widely expressed in various human tissues, localization of (pro)renin receptor protein expression has not yet been systemically determined. Therefore, this study localized (pro)renin receptor protein expression in human organs. Systemic immunohistochemical examination of (pro)renin receptor expression was performed in whole body organs of autopsy cases. (Pro)renin receptor immunostaining was observed in the cytoplasm of cells in almost all human organs. It was observed in thyroid follicular epithelial cells, hepatic cells, pancreatic duct epithelial cells, zona glomerulosa and zona reticularis of the cortex and medulla of the adrenal gland, proximal and distal tubules and collecting ducts of the kidney, cardiomyocytes, and skeletal muscle cells. In the brain, (pro)renin receptor staining was detected in neurons throughout all areas, especially in the medulla oblongata, paraventricular nucleus and supraoptic nucleus of the hypothalamus, cerebrum, granular layer of the hippocampus, Purkinje cell layer of the cerebellum, and the pituitary anterior and posterior lobes. In the anterior lobe of the pituitary gland, all types of anterior pituitary hormone-positive cells showed double staining with (pro)renin receptor. These data showed that (pro)renin receptor protein was expressed in almost all organs of the human body. Its expression pattern was not uniform, and cell-specific expression pattern was observed, supporting the notion that (pro)renin receptor plays numerous physiological roles in each human organ.

Effects of chronic cold exposure on the endothelin system

2006 ◽  
Vol 100 (5) ◽  
pp. 1719-1726 ◽  
Author(s):  
Gin-Fu Chen ◽  
Zhongjie Sun
Keyword(s):  
Epithelial Cells ◽  
Cold Exposure ◽  
Renal Cortex ◽  
Renal Medulla ◽  
Immunohistochemical Analysis ◽  
Receptor Expression ◽  
Mesenteric Arteries ◽  
Receptor Protein ◽  
Cold Temperatures ◽  
Endothelin System

Cold temperatures have adverse effects on the human cardiovascular system. Endothelin (ET)-1 is a potent vasoconstrictor. We hypothesized that cold exposure increases ET-1 production and upregulates ET type A (ETA) receptors. The aim of this study was to determine the effect of cold exposure on regulation of the ET system. Four groups of rats (6–7 rats/group) were used: three groups were exposed to moderate cold (6.7 ± 2°C) for 1, 3, and 5 wk, respectively, and the remaining group was maintained at room temperature (25°C) and served as control. Cold exposure significantly increased ET-1 levels in the heart, mesenteric arteries, renal cortex, and renal medulla. Cold exposure increased ETA receptor protein expression in the heart and renal cortex. ET type B (ETB) receptor expression, however, was decreased significantly in the heart and renal medulla of cold-exposed rats. Cold exposure significantly increased the ratio of ETA to ETB receptors in the heart. An additional four groups of rats (3 rats/group) were used to localize changes in ETA and ETB receptors at 1, 3, and 5 wk of cold exposure. Immunohistochemical analysis showed an increase in ETA, but a decrease in ETB, receptor immunoreactivity in cardiomyocytes of cold-exposed rats. Increased ETA receptor immunoreactivity was also found in vascular smooth muscle cells of cold-exposed rats. Cold exposure increased ETA receptor immunoreactivity in tubule epithelial cells in the renal cortex but decreased ETB receptor immunoreactivity in tubule epithelial cells in the renal medulla. Therefore, cold exposure increased ET-1 production, upregulated ETA receptors, and downregulated ETB receptors.

Abstract 3559: β2-adrenoceptor Protein Expression Is Different Between Buffy Coat And Adipose Tissue

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Kazuko Masuo ◽  
Tomohiro Katsuya ◽  
Hiromi Rakugi ◽  
Ken Sugimoto ◽  
Toshio Ogihara ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Protein Expression ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Leptin Receptor ◽  
Whole Body ◽  
Receptor Protein ◽  
Nerve Activity ◽  
Caucasian Men ◽  
Obese Subjects

Background: Obesity and hypertension are associated with β2-adrenoceptor polymorphisms accompanying with heightened sympathetic nerve activity. In the present study we compared β2-adrenoceptor protein expression between buffy coats (white blood cells as a representive for whole-body) and abdominal subcutaneous fat to further evaluate the contributions of sympathetic nerve activity and β2-adrenoceptor to obesity and hypertension. Methods: In 17 obese normotensive Caucasian men (BMI≥30.0 kg/m2) and 8 age-matched lean Caucasian men (BMI<25 kg/m2), we measured BMI, blood pressure (BP), whole-body plasma norepinephrine (NE) spillover, NE clearance, plasma leptin, and β2-adrenoceptor protein concentration and leptin receptor protein concentration in buffy coats and in abdominal subcutaneous adipose tissue. The β2-adrenoceptor protein expression and leptin receptor protein expression were analysed by Western blotting. Results: Obese subjects had significantly higher whole-body NE spillover (673±245 ng/mL vs. 431±156, P<0.05), plasma leptin (15.2±4.3 ng/mL vs. 4.8±2.4, P<0.01), and BP levels (P<0.05) compared to lean subjects, but the whole-body NE clearance rate was similar. Obese subjects had significantly greater expression of β2-adrenoceptor protein in buffy coats (P<0.05) compared to lean subjects, while they had significantly less β2-adrenoceptor protein expression in abdominal fat (P<0.05). Leptin receptor protein expression in both buffy coats and abdominal fat were greater in obese subjects compared to lean subjects. Conclusions: Obese subjects had greater β2-adrenoceptor protein expression in buffy coats, but less β2-adrenoceptor protein expression in fat. This may suggest that blunted sympathetic nerve activity in adipose tissue (observed by less β2-adrenoceptor protein expression in fat) might relate to obesity and heightened sympathetic nerve activity in whole-body (observed by greater β2-adrenoceptor protein expression in buffy coats and higher NE spillover) may be linked to hypertension. The findings support the concept of selective leptin resistance. Sympathetic nerve activity and β2-adrenoceptor, not leptin, plays an important role is mechanisms of obesity and obesity-related hypertension.

scholarly journals Developmental programming: prenatal androgen excess disrupts ovarian steroid receptor balance

Reproduction ◽  
2009 ◽  
Vol 137 (5) ◽  
pp. 865-877 ◽  
Author(s):  
Hugo H Ortega ◽  
Natalia R Salvetti ◽  
Vasantha Padmanabhan
Keyword(s):  
Protein Expression ◽  
Granulosa Cells ◽  
Steroid Receptor ◽  
Developmental Trajectory ◽  
Receptor Expression ◽  
Model Systems ◽  
Receptor Protein ◽  
Androgen Excess ◽  
Ovarian Steroid ◽  
Prenatal Androgen

Steroid hormones play an important role in reproduction and the receptors through which they signal change in a developmental time, follicle stage, and cell-specific manner. Disruption in steroid receptor expression affects follicle formation and differentiation. In this study, using prenatal testosterone (T) and dihydrotestosterone (DHT)-treated female sheep as model systems, we tested the hypothesis that prenatal androgen excess disrupts the developmental ontogeny of ovarian steroid receptor protein expression. Pregnant Suffolk ewes were injected twice weekly with T propionate or DHT propionate (a non-aromatizable androgen) in cottonseed oil from days 30 to 90 of gestation. Changes in ovarian estrogen receptors (ER; ESR1, ESR2), androgen receptor (AR) and progesterone receptor (PGR) proteins were determined at fetal (days 90 and 140), postpubertal (10 months), and adult (21 months; only prenatal T-treated sheep studied) ages by immunohistochemistry. Prenatal T and DHT treatment induced selective increase in AR but not ER or PGR expression in the stroma and granulosa cells of fetal days 90 and 140 ovaries. An increase in ESR1 and decrease in ESR2 immunostaining coupled with increased AR expression were evident in granulosa cells of antral follicles of 10- and 21-month-old prenatal T but not DHT-treated females (analyzed only at 10 months). These findings provide evidence that an early increase in ovarian AR is the first step in the altered ovarian developmental trajectory of prenatal T-treated females, and manifestations of postnatal ovarian dysfunction are likely facilitated via altered equilibrium of antral follicular granulosa cell ER/AR protein expression.

scholarly journals NIMG-30. PET IMAGING OF ANDROGEN RECEPTOR EXPRESSION IN PATIENTS WITH GBM USING [18F]-FDHT

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii154-ii154
Author(s):  
Anat Mordechai ◽  
Ofer Shamni ◽  
Nomi Zalcman ◽  
Samuel Moscovici ◽  
Alexandre Chicheportiche ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Protein Expression ◽  
Pearson Correlation ◽  
Receptor Expression ◽  
Whole Body ◽  
Normal Brain ◽  
Poor Overall Survival ◽  
Reference Tissue ◽  
Pet Ct ◽  
Tumor Accumulation

Abstract BACKGROUND GBM is associated with poor overall survival partly due to lack of effective treatment. Recently we showed that androgen receptor (AR) protein is overexpressed in 56% of GBM specimens and that AR antagonists induced dose-dependent death in several glioblastoma cell lines. Treatment of mice implanted with human GBM with AR antagonists significantly reduced the growth of the tumor and prolonged the lifespan of the mice. 18f-fluorine-radiolabeled Dihidrotestosteron (DHT), a natural ligand of AR, [16β-18F-fluoro-5α-dihydrotestosterone ([18F]-FDHT)] is one of the PET tracers used to detect AR expression in metastatic prostate cancer. The aim of this study was to identify AR-expressing GBM tumors in real time using PET-CT scan with [18F]-FDHT. MATERIALS AND METHODS Twelve patients with GBM underwent a dynamic (first 30 min) and whole body static (later 60-80 min) [18F]-FDHT PET/CT (296-370 MBq) scans 2-4 days prior to the surgery or biopsy. Protein was extracted from the tumor and subjected to western blot analysis. AR Protein fold change of each tumor sample was calculated by densitometry analysis compared with that of normal brain, following normalization to GAPDH. RESULTS At ~60 min after injection, 6 of the 12 patients showed significantly higher tumor accumulation of [18F]-FDHT, compared to reference tissue (SUV/Control)mean: 1.33-2.63 fold, (SUV/control)max: 1.4-3.43 fold. The patient who had higher tumor accumulation of [18F]-FDHT, demonstrated also high (1.6-2.27 fold/normal brain) AR protein expression within the tumor. Pearson-correlation-coefficient analysis for the (SUV/Control)mean at ~60 min after the injection versus AR protein expression, was positive and significant (R=0.841;p=0.0024). CONCLUSION This study demonstrated for the first time that [18F]-FDHT PET can identify AR-positive-GBM-tumors (with sensitivity and specificity at 100%) and may therefore be a powerful tool to select patients eligible for treatment with AR antagonists. It could possibly be employed also to monitor treatment response and/or progression during the course of therapy.

scholarly journals Beneficial effect of probiotics on Pseudomonas aeruginosa–infected intestinal epithelial cells through inflammatory IL-8 and antimicrobial peptide human beta-defensin-2 modulation

2020 ◽  
Vol 26 (7) ◽  
pp. 592-600
Author(s):  
Fu-Chen Huang ◽  
Yi-Ting Lu ◽  
Yu-Hsuan Liao
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Protein Expression ◽  
Intestinal Epithelial Cells ◽  
Receptor Protein ◽  
Supporting Evidence ◽  
Clinical Effects ◽  
Intestinal Epithelial ◽  
Antibiotic Overuse ◽  
Probiotic Treatment

The human pathogen Pseudomonas aeruginosa can rapidly induce fatal sepsis, even in previously healthy infants or children treated with appropriate antibiotics. To reduce antibiotic overuse, exploring novel complementary therapies, such as probiotics that reportedly protect patients against P. aeruginosa infection, would be particularly beneficial. However, the major mechanism underlying the clinical effects is not completely understood. We thus aimed to investigate how probiotics affect IL-8 and human beta-defensin 2 (hBD-2) in P. aeruginosa–infected intestinal epithelial cells (IECs). We infected SW480 IECs with wild type PAO1 P. aeruginosa following probiotic treatment with Lactobacillus rhamnosus GG or Bifidobacterium longum spp. infantis S12, and analysed the mRNA expression and secreted protein of IL-8 and hBD-2, Akt signalling and NOD1 receptor protein expression. We observed that probiotics enhanced hBD-2 expression but suppressed IL-8 responses when administered before infection. They also enhanced P. aeruginosa–induced membranous NOD1 protein expression and Akt activation. The siRNA-mediated Akt or NOD1 knockdown counteracted P. aeruginosa–induced IL-8 or hBD-2 expression, indicating regulatory effects of these probiotics. In conclusion, these data suggest that probiotics exert reciprocal regulation of inflammation and antimicrobial peptides in P. aeruginosa–infected IECs and provide supporting evidence for applying probiotics to reduce antibiotic overuse.

Early streptozotocin-diabetes mellitus downregulates rat kidney AT2 receptors

2001 ◽  
Vol 280 (2) ◽  
pp. F254-F265 ◽  
Author(s):  
George J. Wehbi ◽  
Joseph Zimpelmann ◽  
Robert M. Carey ◽  
David Z. Levine ◽  
Kevin D. Burns
Keyword(s):  
Diabetic Nephropathy ◽  
Protein Expression ◽  
Mrna Expression ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Receptor Expression ◽  
Receptor Protein ◽  
Ang Ii ◽  
Glomerular Injury ◽  
Early Diabetes

The interaction of ANG II with intrarenal AT1 receptors has been implicated in the progression of diabetic nephropathy, but the role of intrarenal AT2 receptors is unknown. The present studies determined the effect of early diabetes on components of the glomerular renin-angiotensin system and on expression of kidney AT2receptors. Three groups of rats were studied after 2 wk: 1) control (C), 2) streptozotocin (STZ)-induced diabetic (D), and 3) STZ-induced diabetic with insulin implant (D+I), to maintain normoglycemia. By competitive RT-PCR, early diabetes had no significant effect on glomerular mRNA expression for renin, angiotensinogen, or angiotensin-converting enzyme (ACE). In isolated glomeruli, nonglycosylated (41-kDa) AT1 receptor protein expression (AT1A and AT1B) was increased in D rats, with no change in glycosylated (53-kDa) AT1 receptor protein or in AT1 receptor mRNA. By contrast, STZ diabetes caused a significant decrease in glomerular AT2 receptor protein expression (47.0 ± 6.5% of C; P < 0.001; n = 6), with partial reversal in D+I rats. In normal rat kidney, AT2 receptor immunostaining was localized to glomerular endothelial cells and tubular epithelial cells in the cortex, interstitial, and tubular cells in the outer medulla, and inner medullary collecting duct cells. STZ diabetes caused a significant decrease in AT2 receptor immunostaining in all kidney regions, an effect partially reversed in D+I rats. In summary, early diabetes has no effect on glomerular mRNA expression for renin, angiotensinogen, or ACE. AT2 receptors are present in glomeruli and are downregulated in early diabetes, as are all kidney AT2 receptors. Our data suggest that alterations in the balance of kidney AT1 and AT2 receptor expression may contribute to ANG II-mediated glomerular injury in progressive diabetic nephropathy.

ROS and PDFG-β receptors are critically involved in indoxyl sulfate actions that promote vascular smooth muscle cell proliferation and migration

2009 ◽  
Vol 297 (2) ◽  
pp. C389-C396 ◽  
Author(s):  
Hidehisa Shimizu ◽  
Yuichi Hirose ◽  
Fuyuhiko Nishijima ◽  
Yoshiharu Tsubakihara ◽  
Hitoshi Miyazaki
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Nadph Oxidase ◽  
Protein Expression ◽  
Receptor Expression ◽  
Indoxyl Sulfate ◽  
Receptor Protein ◽  
Uremic Toxin ◽  
Diphenylene Iodonium ◽  
Pdgf Stimulation

Patients with chronic renal failure are at greater risk of developing atherosclerosis than healthy individuals, and recent data suggest that the putative uremic toxin indoxyl sulfate (IS) promotes the pathogenesis of atherosclerosis. The present study examined the effects of IS on vascular smooth muscle cells (VSMCs) with respect to reactive oxygen species (ROS), platelet-derived growth factor (PDGF) receptors, and mitogen-activated protein kinases (MAPKs). IS induced the migration and proliferation of VSMCs and synergistically enhanced their PDGF-induced migration as well as proliferation. The effects of PDGF were promoted after a 24-h incubation with IS despite the absence of IS during PDGF stimulation. Intracellular ROS levels were increased in the presence of IS, and PDGF-dependent ROS production was augmented by a prior 24-h incubation with IS even in the absence of IS during PDGF stimulation. These data suggest that IS increases the sensitivity of VSMCs to PDGF. IS also phosphorylated PDGF-β-receptors and upregulated PDGF-β receptor but not α-receptor protein expression in the absence of exogenous PDGF. The NADPH oxidase inhibitor diphenylene iodonium blocked IS-dependent increase in receptor expression. Administration of IS to nephrectomized rats also elevated receptor protein expression in arterial VSMCs. Inhibitors of NADPH oxidase, PDGF-β receptors, extracellular-regulated protein kinase (ERK), and p38 MAPK all inhibited IS-induced VSMCs migration and proliferation. Taken together, these findings indicate that IS induces the migration as well as proliferation of VSMCs through PDGF-β receptors and that ROS generation is critically involved in this process, which promotes the development of atherosclerosis.

scholarly journals SARS-CoV-2 ACE2 and TMPRSS2 Receptor Protein Expression Patterns Throughout Gestation

2021 ◽  
Author(s):  
Drucilla J Roberts ◽  
Lisa M Bebell ◽  
Andrea G Edlow
Keyword(s):  
Protein Expression ◽  
Expression Pattern ◽  
Expression Patterns ◽  
Maternal Blood ◽  
Late Gestation ◽  
Receptor Protein ◽  
Apical Surface ◽  
Third Trimester ◽  
Preliminary Results

Abstract We previously demonstrated that the late gestation placental expression pattern of ACE2 (the primary SARS-CoV-2 receptor) is localized to the villous syncytiotrophoblast (ST), usually in a polarized membranous pattern at the ST base sparing the apical surface (that directly exposed to maternal blood). We found that the late gestation placental expression pattern of TMPRSS2 (the spike proteinase required for SARS-CoV-2 cellular infection), is usually absent in the trophoblast but rarely, weakly expressed in the placental endothelium. We now show the developmental protein expression patterns of ACE2 and TMPRSS2 by immunohistochemistry throughout gestation, from first through third trimester. We found TMPRSS2 expression was rarely detectable in villous endothelium and very rarely detectable in the ST across gestation. We found ACE2 expression varied during gestation with circumferential ST expression more common in early gestations and polarized expression more common in later gestation. Although this study is small, these preliminary results suggest that earlier gestation pregnancies may be more vulnerable to infection than later gestation pregnancies.

scholarly journals TGF-β potentiates airway smooth muscle responsiveness to bradykinin

2005 ◽  
Vol 289 (4) ◽  
pp. L511-L520 ◽  
Author(s):  
Jenny H. Kim ◽  
Deepika Jain ◽  
Omar Tliba ◽  
Bei Yang ◽  
William F. Jester ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Expression ◽  
Airway Smooth Muscle ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Bronchial Hyperresponsiveness ◽  
Calcium Mobilization ◽  
Receptor Expression ◽  
Receptor Protein ◽  
Dependent Manner

The molecular mechanisms by which bradykinin induces excessive airway obstruction in asthmatics remain unknown. Transforming growth factor (TGF)-β has been involved in regulating airway inflammation and remodeling in asthma, although it is unknown whether TGF-β can modulate bradykinin-associated bronchial hyperresponsiveness. To test whether TGF-β directly modulates airway smooth muscle (ASM) responsiveness to bradykinin, isolated murine tracheal rings were used to assess whether TGF-β alters ASM contractile responsiveness to bradykinin. Interestingly, we found TGF-β-treated murine rings (12.5 ng/ml, 18 h) exhibited increased expression of bradykinin 2 (B2) receptors and became hyperreactive to bradykinin, as shown by increases in maximal contractile responses and receptor distribution. We investigated the effect of TGF-β on bradykinin-evoked calcium signals since calcium is a key molecule regulating ASM excitation-contraction coupling. We reported that TGF-β, in a dose- (0.5–10 ng/ml) and time- (2–24 h) dependent manner, increased mRNA and protein expression of the B2 receptor in cultured human ASM cells. Maximal B2 receptor protein expression that colocalized with CD44, a marker of membrane cell surface, occurred after 18 h of TGF-β treatment and was further confirmed using fluorescence microscopy. TGF-β (2.5 ng/ml, 18 h) also increased bradykinin-induced intracellular calcium mobilization in fura-2-loaded ASM cells. TGF-β-mediated enhancement of calcium mobilization was not attenuated with indomethacin, a cyclooxygenase inhibitor. These data demonstrate for the first time that TGF-β may play a role in mediating airway hyperresponsiveness to bradykinin seen in asthmatics by enhancing ASM contractile responsiveness to bradykinin, possibly as a result of increased B2 receptor expression and signaling.

scholarly journals SARS-CoV-2 spike protein promotes IL-6 trans-signaling by activation of angiotensin II receptor signaling in epithelial cells

2020 ◽  
Vol 16 (12) ◽  
pp. e1009128 ◽  
Author(s):  
Tapas Patra ◽  
Keith Meyer ◽  
Lizzie Geerling ◽  
T. Scott Isbell ◽  
Daniel F. Hoft ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Protein Expression ◽  
Organ Damage ◽  
At1 Receptor ◽  
Spike Protein ◽  
Receptor Protein ◽  
Receptor Signaling ◽  
Angiotensin Ii Receptor

Cytokine storm is suggested as one of the major pathological characteristics of SARS-CoV-2 infection, although the mechanism for initiation of a hyper-inflammatory response, and multi-organ damage from viral infection is poorly understood. In this virus-cell interaction study, we observed that SARS-CoV-2 infection or viral spike protein expression alone inhibited angiotensin converting enzyme-2 (ACE2) receptor protein expression. The spike protein promoted an angiotensin II type 1 receptor (AT1) mediated signaling cascade, induced the transcriptional regulatory molecules NF-κB and AP-1/c-Fos via MAPK activation, and increased IL-6 release. SARS-CoV-2 infected patient sera contained elevated levels of IL-6 and soluble IL-6R. Up-regulated AT1 receptor signaling also influenced the release of extracellular soluble IL-6R by the induction of the ADAM-17 protease. Use of the AT1 receptor antagonist, Candesartan cilexetil, resulted in down-regulation of IL-6/soluble IL-6R release in spike expressing cells. Phosphorylation of STAT3 at the Tyr705 residue plays an important role as a transcriptional inducer for SOCS3 and MCP-1 expression. Further study indicated that inhibition of STAT3 Tyr705 phosphorylation in SARS-CoV-2 infected and viral spike protein expressing epithelial cells did not induce SOCS3 and MCP-1 expression. Introduction of culture supernatant from SARS-CoV-2 spike expressing cells on a model human liver endothelial Cell line (TMNK-1), where transmembrane IL-6R is poorly expressed, resulted in the induction of STAT3 Tyr705 phosphorylation as well as MCP-1 expression. In conclusion, our results indicated that the presence of SARS-CoV-2 spike protein in epithelial cells promotes IL-6 trans-signaling by activation of the AT1 axis to initiate coordination of a hyper-inflammatory response.

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