scholarly journals Overexpression of Aquaporin 1 in the Tunica Vaginalis May Contribute to Adult-Onset Primary Hydrocele Testis

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Mami Hattori ◽  
Akiko Tonooka ◽  
Masayoshi Zaitsu ◽  
Koji Mikami ◽  
Ayako Suzue-Yanagisawa ◽  
...  
Keyword(s):  
Water Channel ◽  
Lymphatic Vessels ◽  
Vascular Endothelial ◽  
Adult Onset ◽  
Tunica Vaginalis ◽  
Control Male ◽  
Aqp1 Expression ◽  
Capillary Endothelial Cells ◽  
Hydrocele Testis ◽  
And Control

To investigate the cause of the adult-onset primary noncommunicating hydrocele testis, protein expressions of water channel aquaporins (AQPs) 1 and 3 in the tunica vaginalis were assessed. Frozen tunica vaginalis specimens from patients with adult-onset primary hydrocele testis and control male nonhydrocele patients were subjected to Western blot analysis for the detection of AQP1 and AQP3 proteins. Paraffin-embedded sections of tunica vaginalis specimens were histochemically stained with anti-AQP1 and anti-AQP3 antibodies as well as an anti-podoplanin antibody to stain lymphatic endothelia. Hydrocele fluid was subjected to biochemical analysis. AQP1 protein expression in the tunica vaginalis was significantly higher in patients with adult-onset hydrocele testis than in the controls. The AQP3 protein was not detected in the tunica vaginalis. Histochemically, AQP1 expression in the tunica vaginalis was localized in vascular endothelial and smooth muscle cells. The densities of AQP1-expressing capillaries and lymphatic vessels were similar between the tunica vaginalis of the controls and those of hydrocele patients. Sodium levels were higher in the hydrocele fluid than in the serum. In conclusion, overexpression of the AQP1 protein in individual capillary endothelial cells of the tunica vaginalis may contribute to the development of adult-onset primary noncommunicating hydrocele testis as another aquaporin-related disease.

scholarly journals miR-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via ceRNA crosstalk

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jizhi Wu ◽  
Guangqi Zhang ◽  
Hui Xiong ◽  
Yuguang Zhang ◽  
Gang Ding ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Oxygen Therapy ◽  
Vascular Endothelial Cells ◽  
Inhibitory Effect ◽  
Vascular Endothelial ◽  
Pulmonary Capillaries ◽  
Pulmonary Capillary ◽  
Capillary Endothelial Cells ◽  
Nasal Inhalation ◽  
Induced Apoptosis

AbstractOxygen therapy has been widely used in clinical practice, especially in anesthesia and emergency medicine. However, the risks of hyperoxemia caused by excessive O2 supply have not been sufficiently appreciated. Because nasal inhalation is mostly used for oxygen therapy, the pulmonary capillaries are often the first to be damaged by hyperoxia, causing many serious consequences. Nevertheless, the molecular mechanism by which hyperoxia injures pulmonary capillary endothelial cells (LMECs) has not been fully elucidated. Therefore, we systematically investigated these issues using next-generation sequencing and functional research techniques by focusing on non-coding RNAs. Our results showed that hyperoxia significantly induced apoptosis and profoundly affected the transcriptome profiles of LMECs. Hyperoxia significantly up-regulated miR-181c-5p expression, while down-regulated the expressions of NCAPG and lncRNA-DLEU2 in LMECs. Moreover, LncRNA-DLEU2 could bind complementarily to miR-181c-5p and acted as a miRNA sponge to block the inhibitory effect of miR-181c-5p on its target gene NCAPG. The down-regulation of lncRNA-DLEU2 induced by hyperoxia abrogated its inhibition of miR-181c-5p function, which together with the hyperoxia-induced upregulation of miR-181c-5p, all these significantly decreased the expression of NCAPG, resulting in apoptosis of LMECs. Our results demonstrated a ceRNA network consisting of lncRNA-DLEU2, miR-181c-5p and NCAPG, which played an important role in hyperoxia-induced apoptosis of vascular endothelial injury. Our findings will contribute to the full understanding of the harmful effects of hyperoxia and to find ways for effectively mitigating its deleterious effects.

scholarly journals Successful treatment of hepatic lymphorrhea by percutaneous transhepatic lymphangiography followed by sclerotherapy using OK-432

2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Masayuki Kojima ◽  
Masanori Inoue ◽  
Seiichiro Yamamoto ◽  
Toshio Kanai ◽  
Seishi Nakatsuka ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Rare Case ◽  
Intraperitoneal Administration ◽  
Lymphatic Vessels ◽  
Hepatoduodenal Ligament ◽  
Massive Ascites ◽  
Case Presentation ◽  
Successful Case ◽  
Leakage Site ◽  
And Control

Abstract Background Conventional lymphangiography cannot detect leakage sites of hepatic lymphatic vessels. Percutaneous transhepatic lymphangiography can be used to visualize leakage sites, and once the leakage site has been confirmed, effective sclerotherapy can be performed. Case presentation A rare case of intractable hepatic lymphorrhea due to injury of the hepatoduodenal ligament following pancreaticoduodenectomy is reported. Drainage of massive ascites from the drainage tube continued after surgery. Percutaneous transhepatic lymphangiography visualized the intrahepatic lymphatic vessels and the leakage site at the hepatic hilum. An 8-Fr drainage catheter was inserted adjacent to the leakage point under fluoroscopic computed tomography guidance. Repeated sclerotherapy using intraperitoneal administration of OK-432 (picibanil) through the catheter was performed, which exposed the leakage site, and control of the ascites was finally achieved. Conclusions To the best of our knowledge, this is the first successful case of detection of a leakage site using intrahepatic lymphangiography, followed by sclerotherapy using OK-432.

scholarly journals Human Chorionic Gonadotropin Induces Nestin Expression in Endothelial Cells of the Ovary via Vascular Endothelial Growth Factor Signaling

Endocrinology ◽  
2007 ◽  
Vol 149 (1) ◽  
pp. 253-260 ◽  
Author(s):  
Noriyuki Takahashi ◽  
Masanori T. Itoh ◽  
Bunpei Ishizuka
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Chorionic Gonadotropin ◽  
Growth Factor Signaling ◽  
Vascular Endothelial ◽  
Nestin Expression ◽  
Capillary Endothelial Cells ◽  
Theca Interna ◽  
Endothelial Growth Factor

The intermediate filament protein nestin was originally found to be expressed in neuronal progenitor cells, but recent studies have shown that other cell types, including endocrine and vascular endothelial cells, express nestin. In the present study, we examined the expression and localization of nestin in the ovaries of developing, peripubertal, and adult rats. RT-PCR and Western blot analyses revealed that nestin mRNA and proteins were expressed in adult rat ovaries. Immunohistochemical analyses using adult rat ovaries showed that nestin was mainly localized to capillary endothelial cells of theca interna in follicles with more than two layers of granulosa cells and that its expression increased with follicle growth. Ontogenetically, ovarian nestin expression started at the peripubertal period when the first gonadotropin surge occurs. To test the possibility that gonadotropins induce nestin expression, prepubertal (postnatal d 21) rats were sc injected with equine chorionic gonadotropin (eCG) and/or human chorionic gonadotropin (hCG). A single injection of hCG, but not eCG, was sufficient to induce nestin expression in follicles, mainly in capillary endothelial cells of theca interna. Furthermore, pretreatment with an inhibitor of vascular endothelial growth factor receptor prevented the induction of the nestin expression by hCG. These findings demonstrate that the endogenous LH surge induces nestin expression in capillary endothelial cells of theca interna via the vascular endothelial growth factor signaling pathway. Nestin may be involved in angiogenesis in growing follicles, which is followed by follicle maturation and subsequent ovulation.

Cloning and functional expression of an MIP (AQP0) homolog from killifish (Fundulus heteroclitus) lens

2001 ◽  
Vol 281 (6) ◽  
pp. R1994-R2003 ◽  
Author(s):  
Leila V. Virkki ◽  
Gordon J. Cooper ◽  
Walter F. Boron
Keyword(s):  
Water Permeability ◽  
Fundulus Heteroclitus ◽  
Water Channel ◽  
Fold Increase ◽  
Functional Expression ◽  
Xenopus Laevis Oocytes ◽  
Lens Fiber ◽  
Fiber Cells ◽  
Aqp1 Expression ◽  
Very High

The major intrinsic protein (MIP) of lens fiber cells is a member of the aquaporin (AQP) water channel family. The protein is expressed at very high levels in lens fiber cells, but its physiological function is unclear. By homology to known AQPs, we have cloned a full-length cDNA encoding an MIP from the lens of killifish ( Fundulus heteroclitus). The predicted protein (263 amino acids; GenBank accession no. AF191906 ) shows 77% identity to amphibian MIPs, 70% identity to mammalian MIPs, and 46% identity to mammalian AQP1. Expression of MIPfun in Xenopus laevis oocytes causes an ∼40-fold increase in oocyte water permeability. This stimulation is comparable to that seen with AQP1 and substantially larger than that seen with other MIPs. The mercurials HgCl2 and p-chloromercuribenzenesulfonate inhibit the water permeability of MIPfun by ∼25%. MIPfun is not permeable to glycerol, urea, or formic acid but is weakly permeable to CO2.

scholarly journals Effect of Serum Copper on Circulating Angiogenesis-Related Factors in Women with Preeclampsia

2019 ◽  
Author(s):  
Khalid Najm Nadheer ◽  
Zohreh Zahraei ◽  
Hussein Al-Hakeim
Keyword(s):  
Pregnant Women ◽  
Serum Copper ◽  
Control Group ◽  
Vascular Endothelial ◽  
Related Factors ◽  
Soluble Endoglin ◽  
Iraqi Women ◽  
Endothelial Integrity ◽  
And Control ◽  
Endothelial Growth Factor

Preeclampsia (PE) is characterized by a series of clinical features such as hypertension and proteinuria associated with endothelial dysfunction and the impairment of placenta vascular endothelial integrity. This study aimed to investigate the effect of serum copper (Cu) level on some angiogenesis-related factors including vascular endothelial growth factor-A (VEGF-A), soluble Fms-like tyrosine kinase-1 (sVEGF-R1), soluble endoglin (sEng) and cerruloplasmin (Cp) in Iraqi women with preeclampsia (PE) and control pregnant women. Therefore, 60 women with PE in addition to 30 healthy pregnant women were enrolled in the study. Serum concentration of sEng, VEGF-A, sVEGF-R1, and Cu in PE group significantly increased (p<0.05) in the PE group compared with that in the control group. Increased production of antiangiogenic factors, soluble VEGF-A and sEng contribute to the pathophysiology of PE, indicating the involvement of these parameters in the angiogenic balance in patients with PE. Tests for between-subject effects showed that the circulating angiogenesis factors and Cu were significantly associated with the presence of PE. Serum Cu level was significantly correlated with VEGF- A and VEGF-R1 levels but not with sEng. Multiple regression analysis revealed that only Cp and BP can significantly predict the complications in women with PE. In conclusion, serum Cu has a role in the angiogenesis in women with PE and may be a new drug target in the prevention or treatment of PE.

Expression of vascular endothelial factor-A, gelatinases (MMP-2, MMP-9) and TIMP-1 in uterine leiomyomas

2015 ◽  
Vol 53 (9) ◽  
Author(s):  
Porfyrios Korompelis ◽  
Christina Piperi ◽  
Christos Adamopoulos ◽  
Georgia Dalagiorgou ◽  
Penelope Korkolopoulou ◽  
...  
Keyword(s):  
Prognostic Significance ◽  
Uterine Leiomyomas ◽  
Angiogenic Factor ◽  
Enzyme Linked Immunosorbent Assay ◽  
Vascular Endothelial ◽  
Protein Levels ◽  
Cellular Hypertrophy ◽  
Tissue Specimens ◽  
And Control

AbstractLeiomyomas growth involves cellular hypertrophy, modulation of mitotic activity and upregulation of extracellular matrix (ECM). Vascular factors and matrix metalloproteinases (MMPs) play a coordinated role during neoplasia and tissue remodeling. The present study investigates the role of angiogenic factor vascular endothelial growth factor (VEGF)-A with the activity of main gelatinases, MMP-2/MMP-9 and their tissue inhibitor TIMP-1 in patients with leiomyomas.Peripheral blood of 46 women with uterine leiomyomas was obtained prior hysterectomy to assess VEGF-A, MMP-2, -9, TIMP-1 levels by enzyme-linked immunosorbent assay compared to 39 healthy controls. Protein expression levels of VEGF-A, MMP-2 and MMP-9 were evaluated by western immunoblotting and immunohistochemistry in leiomyomas tissue specimens after hysterectomy. Furthermore, the activity of gelatinases in leiomyoma tissue extracts and control myometrium was evaluated by semi-quantitative zymography.Circulating levels of VEGF-A, MMP-2 and TIMP-1 were significantly elevated in leiomyoma patients compared to controls (p<0.001, p=0.004, p=0.003, respectively). A positive correlation was found between VEGF-A and MMP-2 (p=0.021) as well as MMP-9 (p=0.001) peripheral levels in the patient’s group. Furthermore, increased VEGF-A protein levels were detected in leiomyoma tissue compared to control myometrium, followed by increased localization of both VEGF-A and MMP-2 in the ECM embedding bundles of smooth muscle cells of leiomyomas. The activity of MMP-2 was significantly higher in leiomyomas than normal myometrium in all investigated tissues.This study demonstrates a possible coordinated role of VEGF-A and MMP-2 during uterine leiomyomas growth and angiogenesis with potential prognostic significance.

scholarly journals YAP and TAZ maintain PROX1 expression in the developing lymphatic and lymphovenous valves in response to VEGF-C signaling

Development ◽  
2020 ◽  
Vol 147 (23) ◽  
pp. dev195453
Author(s):  
Boksik Cha ◽  
Yen-Chun Ho ◽  
Xin Geng ◽  
Md. Riaj Mahamud ◽  
Lijuan Chen ◽  
...  
Keyword(s):  
Feedback Loop ◽  
Lymphatic Vessels ◽  
Vascular Endothelial ◽  
Valve Development ◽  
Prox1 Expression ◽  
Homeobox Transcription Factor ◽  
Lymphatic Vasculature ◽  
Factor C ◽  
Endothelial Growth Factor ◽  
First Time

ABSTRACTLymphatic vasculature is an integral part of digestive, immune and circulatory systems. The homeobox transcription factor PROX1 is necessary for the development of lymphatic vessels, lymphatic valves (LVs) and lymphovenous valves (LVVs). We and others previously reported a feedback loop between PROX1 and vascular endothelial growth factor-C (VEGF-C) signaling. PROX1 promotes the expression of the VEGF-C receptor VEGFR3 in lymphatic endothelial cells (LECs). In turn, VEGF-C signaling maintains PROX1 expression in LECs. However, the mechanisms of PROX1/VEGF-C feedback loop remain poorly understood. Whether VEGF-C signaling is necessary for LV and LVV development is also unknown. Here, we report for the first time that VEGF-C signaling is necessary for valve morphogenesis. We have also discovered that the transcriptional co-activators YAP and TAZ are required to maintain PROX1 expression in LVs and LVVs in response to VEGF-C signaling. Deletion of Yap and Taz in the lymphatic vasculature of mouse embryos did not affect the formation of LVs or LVVs, but resulted in the degeneration of these structures. Our results have identified VEGF-C, YAP and TAZ as a crucial molecular pathway in valve development.

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