Abstract MP123: The Fate and Role of Pericytes in Repair and Remodeling of the Infarcted Heart

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Linda Alex ◽  
Ya Su ◽  
Nikolaos G Frangogiannis
Keyword(s):  
Lineage Tracing ◽  
Mrna Levels ◽  
Infarct Zone ◽  
Subsequent Formation ◽  
Mural Cells ◽  
Infarcted Heart ◽  
Reporter Mice ◽  
Ng2 Cells ◽  
Migratory Phenotype

Repair of the infarcted heart is dependent on inflammation-driven activation of myofibroblasts (MFs) and subsequent formation of a scar. Though pericytes have been implicated in injury-associated fibroblast activation in several organs, their potential role in cardiac repair and fibrosis has not been studied. We hypothesized that myocardial infarction (MI) may induce pericyte activation, contributing to repair through pericyte to MF conversion, secretion of fibrogenic mediators, or regulation of angiogenesis. In order to test the hypothesis, we generated pericyte/fibroblast reporter mice (NG2 DsRed ;PDGFRα GFP ). In normal myocardium, NG2 labeled peri-endothelial mural cells that coexpressed PDGFRβ, whereas PDGFRα identified interstitial cells with fibroblast characteristics. Pericytes and fibroblasts had distinct transcriptomic profiles: NG2+/PDGFRα- pericytes expressed αSMA and low amounts of extracellular matrix (ECM) genes, whereas PDGFRα+/NG2- fibroblasts synthesized collagens. Pericyte rarefaction was noted in the necrotic core 3 days after non-reperfused MI. 3-7 days post MI, expansion of the NG2+ population in the infarct zone was associated with emergence of non-mural NG2+/αSMA+ cells with MF characteristics. FACS-sorted NG2+/PDGFRα- cells from 7-day infarcts expressed higher levels of ColIα2 (7.2±1.0-fold) and ColIIIα1 (8.9±1.14-fold), when compared to NG2+/PDGFRα- cells from normal hearts. NG2+ cells had high mRNA levels of integrins α1, αV, β1, and β5, and of MMP14, reflecting an activated migratory phenotype. To examine whether expression of ECM genes by infarct pericytes is due to fibroblast conversion, we did lineage tracing studies using NG2CreER TM ;Rosa tdTomato mice bred with the PDGFRα GFP line for reliable fibroblast identification. 7 days post MI, 5.7%±1.04 of PDGFRα+ fibroblasts were derived from NG2+ cells. Also, αSMA staining showed that 10.49%±2.73 of infarct MFs were derived from NG2+ lineage. The majority of mural cells wrapping neovessels were derived from NG2+ cells, suggesting a role for resident pericytes in infarct angiogenesis. In conclusion, upon MI, pericytes become activated and contribute to repair by undergoing conversion to a subset of myofibroblasts and by coating infarct neovessels.

Abstract 120: Pericytes Contribute To Myofibroblast Expansion And Vascular Maturation In The Infarcted Heart

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Linda Alex ◽  
Kai Su ◽  
Izabela Tuleta ◽  
Nikolaos G Frangogiannis
Keyword(s):  
Lineage Tracing ◽  
Cytokine Gene Expression ◽  
Infarct Zone ◽  
Mural Cell ◽  
Infarcted Myocardium ◽  
Reporter Mice ◽  
Infarct Healing ◽  
Subsequent Activation ◽  
Vascular Maturation

Infarct healing is dependent on recruitment of inflammatory leukocytes and subsequent activation of myofibroblasts (MF) and neovessel formation, ultimately resulting in formation of a highly vascularized collagen-enriched scar. Though the heart has an abundant population of periendothelial pericytes, its role in wound healing upon myocardial infarction (MI) has not been studied. We hypothesized that in the infarcted myocardium, pericytes may become activated, contributing to inflammatory, fibrotic and angiogenic responses. We used pericyte/fibroblast reporter mice (NG2 DsRed ;PDGFRα GFP ), lineage tracing studies and in vitro approaches to study the fate and role of pericytes in the infarcted myocardium. In normal hearts, NG2+/PDGFRα- pericytes and PDGFRα+/NG2- fibroblasts had distinct transcriptomic profiles. Pericytes expressed mural genes like Acta2 , Pdgfrb and low amounts of extracellular matrix (ECM) genes, whereas fibroblasts synthesized collagens, Timp2/3 and matricellular genes. 7 days post-MI, expansion of the NG2+ population in the infarct zone was associated with emergence of non-mural NG2+/αSMA+ cells with MF characteristics. FACS-sorted NG2+/PDGFRα- cells from 7-day infarcts expressed higher levels of collagens when compared to NG2+/PDGFRα- cells from normal hearts. Infarct pericytes had high integrin and MMP14 expression, reflecting an activated migratory phenotype. Lineage tracing using NG2CreER TM ;Rosa tdTomato ;PDGFRα GFP mice showed that 5.7%±1.04 of PDGFRα+ fibroblasts and 10.49%±2.73 of infarct MFs were derived from NG2+ lineage. Pericyte-derived fibroblasts exhibited higher ECM gene synthesis, in comparison to fibroblasts from non-pericyte origin, while pericyte-derived mural cells showed accentuated inflammatory cytokine gene expression. Immunostaining showed pericytes actively contribute to vascular maturation, forming a mural cell coat enwrapping infarct neovessels. In vitro, TGFβ induced integrins, collagens and MMPs in human pericytes, similar to the changes observed in infarct pericytes. Taken together, our evidences show that after MI, pericytes become activated and contribute to repair by undergoing conversion to a subset of myofibroblasts and by coating infarct neovessels.

Abstract MP25: Defining The Role Of Renin Lineage Cells During Regeneration After Release Of Partial Ureteral Obstruction In Neonatal Mice.

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Vidya Nagalakshmi Kusma Harinathan ◽  
Minghong Li ◽  
Ariel R Gomez ◽  
Maria Luisa S Sequeira-Lopez
Keyword(s):  
Ureteral Obstruction ◽  
Unilateral Ureteral Obstruction ◽  
Lineage Tracing ◽  
Kidney Damage ◽  
Regeneration Capacity ◽  
Renal Vasculature ◽  
Dynamic Changes ◽  
Mural Cells ◽  
Neonatal Mice

Our previous study on a partial unilateral ureteral obstruction (pUUO) model in neonatal mice showed that the release of obstruction halts the progression of kidney damage and leads to a remarkable repair of the kidney with improvement in renal blood flow. In the current study, we aim to understand the role of mural cells of the renin lineage during kidney damage and repair in the neonatal pUUO model. Our results show a marked increase in renin-positive areas in kidneys obstructed for 3W (Sham-3W: 0.70±0.10%, n=3; Obstructed-3W: 1.82±0.43%, n=3). However, relief of obstruction at 1W restored the renin-positive areas to sham levels (Post-release-2W: 0.70±0.09%; n=3). Lineage tracing using Ren1 d Cre;mTmG mice revealed a significant increase in GFP+ cells in the obstructed kidneys, with a decrease post-release. To understand further the dynamic changes in cells of renin lineage due to obstruction, we ablated the renin cells using DTA (Diphtheria toxin subunit A). We crossed the DTA fl/fl mice with Ren1 d -DTA het ;Ren1 d Cre;mTmG mice and performed pUUO in the resultant pups with DTA in the renin cells (DTA+). DTA+ animals showed thinning of the renal vasculature and a 90% reduction in renin-positive area compared to controls [Control: 0.70±0.10% (n=3); DTA+: 0.06±0.03% (n=3)]. In addition, there was no significant increase in the renin-positive area post-obstruction [Sham-3W: 0.06±0.04% (n=3); Obstructed-3W: 0.12±0.05% (n=4); Post-release-2W: 0.08±0.03% (n=4)]. These results indicate that ablation of renin cells abolished the obstruction-mediated surge in the renin expression. However, measurement of interstitial collagen positive area indicated that despite the absence of renin cells, the fibrotic damage due to obstruction recovered remarkably post-release [Collagen positive area: Sham-3W: 3.38±0.67% (n=3) Obstructed-3W: 62.98±31.50% (n=3); Post-release-2W: 10.93±5.46% (n=4)]. Similarly, vascular damage induced by persistent obstruction and recovery following the relief of obstruction was similar between the DTA+ and non-DTA animals. Our results imply that though the renin and renin lineage cells increase in obstructed kidneys, ablation of renin cells does not affect the regeneration capacity of kidneys following the relief of obstruction.

Abstract WP322: Do Mural Cells Differentiate Into Microglia-Like Cells After Ischemic Stroke?

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Yao Yao ◽  
Abhijit Nirwane
Keyword(s):  
Ischemic Stroke ◽  
Substantial Reduction ◽  
Transgenic Animals ◽  
Artery Occlusion ◽  
Lineage Tracing ◽  
Future Research ◽  
Mural Cells ◽  
Reporter Mice ◽  
Cerebral Artery Occlusion ◽  
The Brain

Introduction: Controversial results exist on whether mural cells can differentiate into microglia-like cells after ischemic stroke. This discrepancy can be due to different experimental methods (immunostaining versus lineage tracing) and/or distinct transgenic animals (RGS5 GFP versus Tbx18-CreERT mice). Methods: To determinate whether mural cells are able to differentiate into microglia-like cells after ischemic stroke, we permanently labeled mural cells with tdTomato by crossing PDGFRβ-Cre and PDGFRβ-CreERT with Ai14 reporter mice. The resulting Ai14:PDGFRβ-Cre + and Ai14:PDGFRβ-CreERT + mice were subjected to 45 minutes of middle cerebral artery occlusion (MCAO) followed by reperfusion. At various time points after injury, the proliferation, apoptosis, and differentiation of PDGFRβ + cells were examined. Results: In both Ai14:PDGFRβ-Cre + and Ai14:PDGFRβ-CreERT + mice, we observed a substantial reduction of PDGFRβ + cells at day 2 after ischemic stroke and a subsequent repopulation (mainly due to proliferation) of PDGFRβ + cells at day 7 after ischemic stroke. We also showed that PDGFRβ + cells changed their morphology and differentiated into microglia-like cells at day 7 after injury, suggesting that PDGFRβ + cells can indeed differentiate into microglia-like cells after ischemic stroke. In addition, we noted that PDGFRβ also labeled Col1α1 + fibroblasts in the brain. Interestingly, high numbers of PDGFRβ + Col1α1 + cells were found in both Ai14:PDGFRβ-Cre + and Ai14:PDGFRβ-CreERT + mice at day 7 after ischemic injury. Conclusions: These results suggest that PDGFRβ is not an ideal marker for mural cells in pathological conditions that involve fibroblast activation. It remains unclear whether mural cells or fibroblasts differentiate into microglia-like cells after ischemic stroke. Future research should focus on answering this important question.

scholarly journals Selective and inducible targeting of CD11b+mononuclear phagocytes in the murine lung with hCD68-rtTA transgenic systems

2016 ◽  
Vol 311 (1) ◽  
pp. L87-L100 ◽  
Author(s):  
Alexandra L. McCubbrey ◽  
Lea Barthel ◽  
Kara J. Mould ◽  
Michael P. Mohning ◽  
Elizabeth F. Redente ◽  
...  
Keyword(s):  
Lineage Tracing ◽  
Mononuclear Phagocytes ◽  
Acute Lung Inflammation ◽  
Unique Role ◽  
Murine Lung ◽  
Disease States ◽  
Reporter Mice ◽  
Gfp Reporter ◽  
Low Levels

During homeostasis two distinct macrophage (Mø) populations inhabit the lungs: tissue Mø (often called interstitial Mø) and resident alveolar Mø (resAMø). During acute lung inflammation, monocytes from the circulation migrate to areas of injury where they mature into a third Mø population: recruited Mø. Resident AMø uniquely express low levels of CD11b and high levels of CD11c. In comparison, recruited Mø and tissue Mø express high levels of CD11b and low levels of CD11c. It is likely that these three Mø subpopulations play distinct roles in injury and disease states; however, tools with which to individually target or track these populations are lacking. Here we demonstrate the utility of an hCD68-rtTA transgenic system for specific, robust, and inducible targeting of CD11b+recruited Mø and tissue Mø in the murine lung with negligible activation in resAMø. Using hCD68rtTA-GFP reporter mice, we show both during homeostasis and inflammation that administration of doxycycline induces tet-On reporter expression in recruited Mø and tissue Mø but not in resident AMø. We further demonstrate how hCD68-rtTA can be effectively combined with tet-On Cre to target these same recMø and tissue Mø. Accordingly, the hCD68-rtTA system is a powerful new tool that can be used for lineage tracing, fate mapping, and gene deletion in a variety of murine models, thereby enabling sophisticated investigation of the unique role of these CD11b+Mø during lung heath and disease.

scholarly journals Myh11+ microvascular mural cells and derived mesenchymal stem cells promote retinal fibrosis

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
H. Clifton Ray ◽  
Bruce A. Corliss ◽  
Anthony C. Bruce ◽  
Sam Kesting ◽  
Paromita Dey ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Scar Tissue ◽  
Lineage Tracing ◽  
Ocular Injury ◽  
Myofibroblast Differentiation ◽  
Subsequent Formation ◽  
Mural Cells ◽  
Collagen Secretion ◽  
Retinal Microvasculature

Abstract Retinal diseases are frequently characterized by the accumulation of excessive scar tissue found throughout the neural retina. However, the pathophysiology of retinal fibrosis remains poorly understood, and the cell types that contribute to the fibrotic response are incompletely defined. Here, we show that myofibroblast differentiation of mural cells contributes directly to retinal fibrosis. Using lineage tracing technology, we demonstrate that after chemical ocular injury, Myh11+ mural cells detach from the retinal microvasculature and differentiate into myofibroblasts to form an epiretinal membrane. Inhibition of TGFβR attenuates Myh11+ retinal mural cell myofibroblast differentiation, and diminishes the subsequent formation of scar tissue on the surface of the retina. We demonstrate retinal fibrosis within a murine model of oxygen-induced retinopathy resulting from the intravitreal injection of adipose Myh11-derived mesenchymal stem cells, with ensuing myofibroblast differentiation. In this model, inhibiting TGFβR signaling does not significantly alter myofibroblast differentiation and collagen secretion within the retina. This work shows the complexity of retinal fibrosis, where scar formation is regulated both by TGFβR and non-TGFβR dependent processes involving mural cells and derived mesenchymal stem cells. It also offers a cautionary note on the potential deleterious, pro-fibrotic effects of exogenous MSCs once intravitreally injected into clinical patients.

Abstract 23: Foxd1+ Stromal Cells, the Required Progenitors for Kidney Vascular Development

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Eugene E Lin ◽  
Roberto A Gomez ◽  
Maria-Luisa S Sequeira-Lopez
Keyword(s):  
Stromal Cells ◽  
Mesangial Cells ◽  
Cell Types ◽  
Lineage Tracing ◽  
Arterial Tree ◽  
Mural Cell ◽  
Mural Cells ◽  
Selective Ablation ◽  
Similar Phenotype

The mechanisms underlying the establishment, assembly and maintenance of the renal blood vessels are poorly understood. We have previously suggested using detailed lineage tracing that renal stromal cells, characterized by their early and transient expression of the transcription factor Foxd1 , give rise to the entirety of the mural cell layer of the renal arterial tree and mesangial cells. Mural cells as defined here exclude endothelial cells, which we identified as having a separate precursor, the renal hemangioblast. To define whether Foxd1 cells are the required essential progenitor or whether their role as such could be assumed by other cell types, we used the cre-lox system to generate mice expressing diphtheria toxin subunit A in Foxd1+ cells ( Foxd1-DTA mice ) which resulted in animals with selective ablation of Foxd1+ cells. Kidneys from Foxd1-DTA embryos had a significantly reduced complement of arterial mural cells, lacking smooth muscle cells, perivascular fibroblasts, renin cells and mesangial cells. Interestingly, the few vessels that remained were also abnormal: they originated underneath the kidney capsule and elongated towards the center of the kidney rather than radiating outward from the center of the kidney. In addition, ablation of Foxd1 cells resulted in significantly delayed nephrogenesis and reduction in glomerular number. In conjunction with our previous data showing a similar phenotype upon global deletion of the Foxd1 ,gene, this illustrates the central role of Foxd1 and the cells that express it during early development. We conclude that Foxd1 stromal cells are the required progenitors for the establishment of the mural cells of the kidney arterioles and (via Foxd1 expression) for the proper origin and orientation of the kidney vessels.

scholarly journals Validation of Specific and Reliable Genetic Tools to Identify, Label, and Target Cardiac Pericytes in Mice

2021 ◽  
Author(s):  
Linda Alex ◽  
Izabela Tuleta ◽  
Venugopal Harikrishnan ◽  
Nikolaos G. Frangogiannis
Keyword(s):  
Large Population ◽  
Growth Factor Receptor ◽  
Cell Types ◽  
Lineage Tracing ◽  
Matricellular Proteins ◽  
Mural Cells ◽  
Reporter Mice ◽  
Fibrillar Collagens ◽  
Dual Reporter ◽  
Genes Encoding

Background In the myocardium, pericytes are often confused with other interstitial cell types, such as fibroblasts. The lack of well‐characterized and specific tools for identification, lineage tracing, and conditional targeting of myocardial pericytes has hampered studies on their role in heart disease. In the current study, we characterize and validate specific and reliable strategies for labeling and targeting of cardiac pericytes. Methods and Results Using the neuron‐glial antigen 2 (NG2) DsRed reporter line, we identified a large population of NG2+ periendothelial cells in mouse atria, ventricles, and valves. To examine possible overlap of NG2+ mural cells with fibroblasts, we generated NG2 DsRed ; platelet‐derived growth factor receptor (PDGFR) α EGFP pericyte/fibroblast dual reporter mice. Myocardial NG2+ pericytes and PDGFRα+ fibroblasts were identified as nonoverlapping cellular populations with distinct transcriptional signatures. PDGFRα+ fibroblasts expressed high levels of fibrillar collagens, matrix metalloproteinases, tissue inhibitor of metalloproteinases, and genes encoding matricellular proteins, whereas NG2+ pericytes expressed high levels of Pdgfrb , Adamts1 , and Vtn . To validate the specificity of pericyte Cre drivers, we crossed these lines with PDGFRα EGFP fibroblast reporter mice. The constitutive NG2 Cre driver did not specifically track mural cells, labeling many cardiomyocytes. However, the inducible NG2 CreER driver specifically traced vascular mural cells in the ventricle and in the aorta, without significant labeling of PDGFRα+ fibroblasts. In contrast, the inducible PDGFRβ CreER line labeled not only mural cells but also the majority of cardiac and aortic fibroblasts. Conclusions Fibroblasts and pericytes are topographically and transcriptomically distinct populations of cardiac interstitial cells. The inducible NG2 CreER driver optimally targets cardiac pericytes; in contrast, the inducible PDGFRβ CreER line lacks specificity.

Abstract 13911: Interleukin-5-induced Eosinophil Population Improves Cardiac Function After Myocardial Infarction

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Jun-Yan Xu ◽  
Wen-Yang Jiang ◽  
Yu-Yan Xiong ◽  
Rui-Jie Tang ◽  
Yu Ning ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Western Blot ◽  
Macrophage Polarization ◽  
M2 Macrophages ◽  
Infarct Zone ◽  
Infarcted Myocardium ◽  
Infarcted Heart

Background: Eosinophils have been commonly recognized as one of the major participants in helminth infection and allergic diseases. Recent studies suggest that these innate immune cells mediate tissue repairs after muscle, hepatic, or endometrial injuries. Yet, the precise role of eosinophils in myocardial infarction (MI) remains unclear. Interleukin (IL)-5 is the most important cytokines that are responsible for the development, activation, and survival of eosinophils. Here, we report a role of IL-5 in infarcted heart. Methods and Results: MI was induced by permanent ligation of left anterior descending coronary artery in wild-type C57BL/6 mice. Western blot show that infarcted heart IL-5 expression is increased by 2.35-fold (P<0.01) higher than their expression in the heart of sham mice at day 5 after surgery. External supply of recombinant mouse IL-5 (100 μg/kg/day for 3 days) reduces the infarct size (by 13.38%, P<0.01), increases ejection fraction (from 32.41% to 43.93%, P<0.01), and increases angiogenesis (CD31 area from 3.35% to 4.14%, P=0.03) in the peri-infarct zone. An expansion of eosinophils is observed in both the peripheral blood and infarcted myocardium after IL-5 administration. Pharmacological depletion of eosinophils by TRFK5 pretreatment mutes the beneficial effects of IL-5 in MI mice. Mechanistic studies also demonstrate that IL-5 increases the accumulation of M2 macrophages in infarcted myocardium at day 7 post-MI. In vitro co-culture experiments reveal that eosinophils shift bone marrow-derived macrophage polarization towards the M2 phenotypes. This effect is abolished by IL-4 neutralizing antibody, but not IL-10 or IL-13 neutralization. Western blot analyses show that eosinophils promote the macrophage downstream STAT6 phosphorylation. Conclusions: We demonstrate here that IL-5 facilitates the recovery of post-MI cardiac function by promoting eosinophils accumulation and subsequent polarization of M2 macrophages via the IL-4/STAT6 axis.

scholarly journals CD206+ macrophage is an accelerator of endometriotic-like lesion via promoting angiogenesis in the endometriosis mouse model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yosuke Ono ◽  
Osamu Yoshino ◽  
Takehiro Hiraoka ◽  
Erina Sato ◽  
Akiko Furue ◽  
...  
Keyword(s):  
Mouse Model ◽  
Diphtheria Toxin ◽  
Immunohistochemical Study ◽  
Mrna Levels ◽  
Cytokines And Chemokines ◽  
Diphtheria Toxin Receptor ◽  
Endothelial Cell Marker ◽  
Toxin Receptor ◽  
Group A

AbstractIn endometriosis, M2 MΦs are dominant in endometriotic lesions, but the actual role of M2 MΦ is unclear. CD206 positive (+) MΦ is classified in one of M2 type MΦs and are known to produce cytokines and chemokines. In the present study, we used CD206 diphtheria toxin receptor mice, which enable to deplete CD206+ cells with diphtheria toxin (DT) in an endometriosis mouse model. The depletion of CD206+ MΦ decreased the total weight of endometriotic-like lesions significantly (p < 0.05). In the endometriotic-like lesions in the DT group, a lower proliferation of endometriotic cells and the decrease of angiogenesis were observed. In the lesions, the mRNA levels of VEGFA and TGFβ1, angiogenic factors, in the DT group significantly decreased to approximately 50% and 30% of control, respectively. Immunohistochemical study revealed the expressions of VEGFA and an endothelial cell marker CD31 in lesions of the DT group, were dim compared to those in control. Also, the number of TGFβ1 expressing MΦ was significantly reduced compared to control. These data suggest that CD206+ MΦ promotes the formation of endometriotic-like lesions by inducing angiogenesis around the lesions.

scholarly journals Longitudinal Expression of Testicular TAS1R3 from Prepuberty to Sexual Maturity in Congjiang Xiang Pigs

Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 437
Author(s):  
Ting Gong ◽  
Weiyong Wang ◽  
Houqiang Xu ◽  
Yi Yang ◽  
Xiang Chen ◽  
...  
Keyword(s):  
Sexual Maturity ◽  
Cell Function ◽  
Expression Patterns ◽  
Taste Receptor ◽  
Receptor Type ◽  
Mrna Levels ◽  
Early Puberty ◽  
Specific Expression

Testicular expression of taste receptor type 1 subunit 3 (T1R3), a sweet/umami taste receptor, has been implicated in spermatogenesis and steroidogenesis in mice. We explored the role of testicular T1R3 in porcine postnatal development using the Congjiang Xiang pig, a rare Chinese miniature pig breed. Based on testicular weights, morphology, and testosterone levels, four key developmental stages were identified in the pig at postnatal days 15–180 (prepuberty: 30 day; early puberty: 60 day; late puberty: 90 day; sexual maturity: 120 day). During development, testicular T1R3 exhibited stage-dependent and cell-specific expression patterns. In particular, T1R3 levels increased significantly from prepuberty to puberty (p < 0.05), and expression remained high until sexual maturity (p < 0.05), similar to results for phospholipase Cβ2 (PLCβ2). The strong expressions of T1R3/PLCβ2 were observed at the cytoplasm of elongating/elongated spermatids and Leydig cells. In the eight-stage cycle of the seminiferous epithelium in pigs, T1R3/PLCβ2 levels were higher in the spermatogenic epithelium at stages II–VI than at the other stages, and the strong expressions were detected in elongating/elongated spermatids and residual bodies. The message RNA (mRNA) levels of taste receptor type 1 subunit 1 (T1R1) in the testis showed a similar trend to levels of T1R3. These data indicate a possible role of T1R3 in the regulation of spermatid differentiation and Leydig cell function.

Sign in / Sign up

Export Citation Format

Share Document