Different expressions of aquaporin water channels and macrophages infiltration in human cervix remodeling during pregnancy

2021 ◽  
Author(s):  
Jinying Yang ◽  
Shengjun Yu ◽  
Guanglan Zhang ◽  
Zheng Zheng ◽  
Ping Li ◽  
...  
Keyword(s):  
Water Content ◽  
Critical Role ◽  
Water Channels ◽  
Female Reproductive Tract ◽  
Macrophage Infiltration ◽  
Cervical Ripening ◽  
Aqp4 Expression ◽  
Cervical Stroma ◽  
Perivascular Area ◽  
Human Cervix

Abstract Despite aquaporin water channels (AQPs) play a critical role in maintaining water homeostasis in female reproductive tract and prompt a gradual increase in water content in cervical edema as pregnancy progressed, their relationship with macrophage infiltration and collagen content in human cervical remodeling need to be further investigated. This is the first study to examine the expression and localization of AQP3, AQP4, AQP5, AQP8 and macrophages simultaneously in human cervical ripening. The immunoreactivity of these AQPs was 2.6 to 6-fold higher on gestational weeks 26 (GD26W) than that on GD6W and GD15W, but AQP4 expression on GD39W dropped a similar extent on GD15W, other AQPs continued to rise on GD39W. The AQP3, AQP4 and AQP5 intensity seemed more abundant in cervical stroma than in the perivascular area on GD26W; the distribution of AQP3, AQP5 and AQP8 in cervical stroma was equivalent to that in the perivascular area on GD39W. Macrophage numbers were 1.7-fold higher in subepithelium region and 3.0-fold higher in center area on GD26W than that on GD15W; such numbers remained elevated on GD39W. The electron micrographs showed that cervical extensibility increased significantly on GD26W and GD39W accompanied with increased macrophage infiltration, cervical water content and much more space among collagen fibers. These findings suggest that the upregulation of AQPs expression in human cervix is closely related to enhanced macrophage infiltration during pregnancy; there may be a positive feedback mechanism between them to lead the increase of water content and the degradation of collagen.

Essential role of PKC-ζ in normal and angiotensin II-accelerated neointimal growth after vascular injury

2006 ◽  
Vol 291 (4) ◽  
pp. H1602-H1613 ◽  
Author(s):  
Jean-Hugues Parmentier ◽  
Chunxiang Zhang ◽  
Anne Estes ◽  
Susan Schaefer ◽  
Kafait U. Malik
Keyword(s):  
Smooth Muscle ◽  
Vascular Injury ◽  
Critical Role ◽  
Immunohistochemical Analysis ◽  
Vascular Wall ◽  
Ang Ii ◽  
Neointimal Formation ◽  
Monocyte Chemoattractant Protein 1 ◽  
Perivascular Area ◽  
Pkc Ζ

The contribution of atypical protein kinase C (PKC)-ζ to ANG II-accelerated restenosis after endoluminal vascular injury was investigated by using the rat carotid balloon injury model. Exposure of injured arteries to ANG II resulted in an extensive neointimal thickening (1.9 times) compared with vehicle at day 14. Treatment with PKC-ζ antisense, but not scrambled, oligonucleotides reduced neointimal formation observed in the presence or absence of ANG II. Examination of early events (2 days) after injury showed an increase in cellularity in the perivascular area of the artery wall that was transferred to the adventitia and media after exposure to ANG II, events blocked by PKC-ζ antisense, but not scrambled, oligonucleotides. A positive correlation between medial cellularity at day 2 and extent of neointimal growth at day 14 was established. Immunohistochemical analysis showed that upregulation of inflammatory markers after injury, as well as infiltration of ED1+monocytes/macrophages from the perivascular area to the adventitia, was accelerated by ANG II. However, ANG II-stimulated medial increase in cellularity was proliferation independent, and these cells were monocyte chemoattractant protein-1+/vimentin+but ED1−/VCAM−. PKC-ζ is degraded after injury, and inhibition of its neosynthesis in medial vascular smooth muscle cells or in infiltrating cells with PKC-ζ antisense attenuated medial cellularity and expression of inflammation mediators without reversing smooth muscle cell dedifferentiation. Together, these data indicate that PKC-ζ plays a critical role in normal and ANG II-accelerated neointimal growth through a mechanism involving upregulation of inflammatory mediators, leading to cell infiltration in the media of the vascular wall.

In vivo inhibition of transcellular water channels (aquaporin-1) during acute peritoneal dialysis in rats

1996 ◽  
Vol 271 (6) ◽  
pp. H2254-H2262 ◽  
Author(s):  
O. Carlsson ◽  
S. Nielsen ◽  
el-R. Zakaria ◽  
B. Rippe
Keyword(s):  
Peritoneal Dialysis ◽  
Water Transport ◽  
Water Flow ◽  
Peritoneal Cavity ◽  
Critical Role ◽  
Water Channels ◽  
Capillary Endothelium ◽  
Tissue Fixation ◽  
Solute Permeability ◽  
Aquaporin 1

During peritoneal dialysis (PD), a major portion of the osmotically induced water transport to the peritoneum can be predicted to occur through endothelial water-selective channels. Aquaporin-1 (AQP-1) has recently been recognized as the molecular correlate to such channels. Aquaporins can be inhibited by mercurials. In the present study, HgCl2 was applied locally to the peritoneal cavity in rats after short-term tissue fixation, used to protect the tissues from HgCl2 damage. Dianeal (3.86%) was employed as dialysis fluid, 125I-albumin as an intraperitoneal volume marker, and 51Cr-EDTA (constantly infused intravenously) to assess peritoneal small-solute permeability characteristics. Immunocytochemistry and immunoelectron microscopy revealed abundant AQP-1 labeling in capillary endothelium in peritoneal tissues, representing sites for HgCl2 inhibition of water transport. HgCl2 treatment reduced water flow and inhibited the sieving of Na+ without causing any untoward changes in microvascular permeability, compared with that of fixed control rats, in which the peritoneal cavity was exposed to tissue fixation alone. In fixed control rats, the mean intraperitoneal volume (IPV) increased from 20.5 +/- 0.15 to 25.0 +/- 0.52 ml in 60 min, whereas in the HgCl2-treated rats, the increment was only from 20.7 +/- 0.23 to 23.5 +/- 0.4 ml. In fixed control rats, the dialysate Na+ fell from 135.3 +/- 0.97 to 131.3 +/- 1.72 mM, whereas in the HgCl2-treated rats the dialysate Na+ concentration remained unchanged between 0 and 40 min, further supporting that water channels had been blocked. Computer simulations of peritoneal transport were compatible with a 66% inhibition of water flow through aquaporins. The observed HgCl2 inhibition of transcellular water channels strongly indicates a critical role of aquaporins in PD and provides evidence that water channels are crucial in transendothelial water transport when driven by crystalloid osmosis.

Brain edema after intracerebral hemorrhage in rats: the role of iron overload and aquaporin 4

2009 ◽  
Vol 110 (3) ◽  
pp. 462-468 ◽  
Author(s):  
Wang Gai Qing ◽  
Yang Qi Dong ◽  
Tang Qing Ping ◽  
Li Guang Lai ◽  
Li Dong Fang ◽  
...  
Keyword(s):  
Iron Overload ◽  
Water Content ◽  
Brain Edema ◽  
Time Course ◽  
Iron Chelator ◽  
Brain Water Content ◽  
Edema Formation ◽  
Aqp4 Expression ◽  
The Right ◽  
Brain Water

Object Brain edema formation following intracerebral hemorrhage (ICH) appears to be partly related to erythrocyte lysis and hemoglobin release. An increase of brain water content was associated with an increase of brain iron, which is an erythrocyte degradation product. Expression of AQP4 is highly modified in several brain disorders, and it can play a key role in cerebral edema formation. However, the question whether AQP4 is regulated by drugs lacks reliable evidence, and the interacting roles of iron overload and AQP4 in brain edema after ICH are unknown. The goal of this study was to clarify the relationship between iron overload and AQP4 expression and to characterize the effects of the iron chelator deferoxamine (DFO) on delayed brain edema after experimental ICH. Methods A total of 144 Sprague-Dawley rats weighing between 250 and 300 g were used in this work. The animals were randomly divided into 4 groups. The ICH models (Group C) were generated by injecting 100 μl autologous blood stereotactically into the right caudate nucleus; surgical control rats (Group B) were generated in a similar fashion, by injecting 100 μl saline into the right caudate nucleus. Intervention models (Group D) were established by intraperitoneal injection of DFO into rats in the ICH group. Healthy rats (Group A) were used for normal control models. Brain water content, iron deposition, and AQP4 in perihematomal brain tissue were evaluated over the time course of the study (1, 3, 7, and 14 days) in each group. Results Iron deposition was found in the perihematomal zone as early as the 1st day after ICH, reaching a peak after 7 days and remaining at a high level thereafter for at least 14 days following ICH. Rat brain water content around the hematoma increased progressively over the time course, reached its peak at Day 3, and still was evident at Day 7 post-ICH. Immunohistochemical analysis showed that AQP4 was richly expressed over glial cell processes surrounding microvessels in the rat brain; there was upregulation of the AQP4 expression in perihematomal brain during the observation period, and it reached maximum at 3 to 7 days after ICH. The changes of brain water content were accompanied by an alteration of AQP4. The application of the iron chelator DFO significantly reduced iron overload, brain water content, and AQP4 level in the perihematomal area compared with the control group. Conclusions Iron overload and AQP4 may play a critical role in the formation of brain edema after ICH. In addition, AQP4 expression was affected by iron concentration. Importantly, treatment with DFO significantly reduced brain edema in rats and inhibited the AQP4 upregulation after ICH. Deferoxamine may be a potential therapeutic agent for treating ICH.

Mechanical Signaling and Extracellular Matrix in Uterine Fibroids

2017 ◽  
Vol 35 (06) ◽  
pp. 487-493 ◽  
Author(s):  
Saima Rafique ◽  
James Segars ◽  
Phyllis Leppert
Keyword(s):  
Gene Expression ◽  
Extracellular Matrix ◽  
Reproductive Tract ◽  
Critical Role ◽  
Uterine Fibroids ◽  
Female Reproductive Tract ◽  
Benign Tumors ◽  
Mechanical Signaling ◽  
Abnormal Cells ◽  
Fibroid Growth

AbstractFibroids (uterine leiomyomas) are the most common benign tumors of the female reproductive tract. Steroid hormones, growth factors, and cytokines have long been implicated in fibroid growth; however, research suggests that changes in the extracellular matrix and mechanical signaling play a critical role in fibroid growth and differentiation. Studies have shown that growth of fibroids is related to the change in the volume and composition of extracellular matrix with increased deposition of abnormal collagen, glycoproteins, laminins, fibronectins, and an increased osmotic stress. These changes generate mechanical stress which is converted to chemical signals in the cells through mechanotransduction and eventually affects gene expression and protein synthesis. Current studies also suggest that mechanical signaling in fibroid cells is abnormal as evidenced by decreased apoptosis of abnormal cells and deposition of a stiff extracellular matrix promoting fibrosis. Understanding and defining these mechanisms could help design new therapies for the treatment of fibroids.

scholarly journals Lost Polarization of Aquaporin4 and Dystroglycan in the Core Lesion after Traumatic Brain Injury Suggests Functional Divergence in Evolution

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Hui Liu ◽  
Gou ping Qiu ◽  
Fei Zhuo ◽  
Wei hua Yu ◽  
Shan quan Sun ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Early Stage ◽  
Functional Divergence ◽  
Edema Formation ◽  
Aqp4 Expression ◽  
The Core ◽  
Perivascular Area ◽  
Brain Edema Formation

Objective. To understand how aquaporin4 (AQP4) and dystroglycan (DG) polarized distribution change and their roles in brain edema formation after traumatic brain injury (TBI).Methods. Brain water content, Evans blue detection, real-time PCR, western blot, and immunofluorescence were used.Results. At an early stage of TBI, AQP4 and DG maintained vessel-like pattern in perivascular endfeet; M1, M23, and M1/M23 were increased in the core lesion. At a later stage of TBI, DG expression was lost in perivascular area, accompanied with similar but delayed change of AQP4 expression; expression of M1, M23, and DG and the ratio of M1/M2 were increased.Conclusion. At an early stage, AQP4 and DG maintained the polarized distribution. Upregulated M1 and M23 could retard the cytotoxic edema formation. At a later stage AQP4 and DG polarized expression were lost from perivascular endfeet and induced the worst cytotoxic brain edema. The alteration of DG expression could regulate that of AQP4 expression after TBI.

Immunohistochemical determination of thioredoxin and glutaredoxin distribution in the human cervix ,and possible relation to cervical ripening

2003 ◽  
Vol 17 (4) ◽  
pp. 303-310
Author(s):  
J. Lysell ◽  
Y. Stjernholm Vladic ◽  
N. Ciarlo ◽  
A. Holmgren ◽  
L. Sahlin
Keyword(s):  
Cervical Ripening ◽  
Human Cervix

scholarly journals Ulinastatin Suppresses Burn-Induced Lipid Peroxidation and Reduces Fluid Requirements in a Swine Model

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Hong-Min Luo ◽  
Ming-Hua Du ◽  
Zhi-Long Lin ◽  
Quan Hu ◽  
Lin Zhang ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Water Content ◽  
Critical Role ◽  
Thiobarbituric Acid ◽  
Swine Model ◽  
Fluid Accumulation ◽  
Lung Water ◽  
Miniature Swine ◽  
Tissue Water ◽  
Pulmonary Vascular Permeability

Objective. Lipid peroxidation plays a critical role in burn-induced plasma leakage, and ulinastatin has been reported to reduce lipid peroxidation in various models. This study aims to examine whether ulinastatin reduces fluid requirements through inhibition of lipid peroxidation in a swine burn model.Methods. Forty miniature swine were subjected to 40% TBSA burns and were randomly allocated to the following four groups: immediate lactated Ringer's resuscitation (ILR), immediate LR containing ulinastatin (ILR/ULI), delayed LR resuscitation (DLR), and delayed LR containing ulinastatin (DLR/ULI). Hemodynamic variables, net fluid accumulation, and plasma thiobarbituric acid reactive substances (TBARS) concentrations were measured. Heart, liver, lung, skeletal muscle, and ileum were harvested at 48 hours after burn for evaluation of TBARS concentrations, activities of antioxidant enzymes, and tissue water content.Results. Ulinastatin significantly reduced pulmonary vascular permeability index (PVPI) and extravascular lung water index (ELWI), net fluid accumulation, and water content of heart, lung, and ileum in both immediate or delayed resuscitation groups. Furthermore, ulinastatin infusion significantly reduced plasma and tissue concentrations of TBARS in both immediate or delayed resuscitation groups.Conclusions. These results indicate that ulinastatin can reduce fluid requirements through inhibition of lipid peroxidation.

scholarly journals Cervical remodeling in term and preterm birth: insights from an animal model

Reproduction ◽  
2012 ◽  
Vol 143 (4) ◽  
pp. 429-438 ◽  
Author(s):  
Mala Mahendroo
Keyword(s):  
Preterm Birth ◽  
Immune Cells ◽  
Normal Pregnancy ◽  
Cervical Ripening ◽  
Tissue Stiffness ◽  
Cervical Remodeling ◽  
Subsequent Loss ◽  
Pregnancy And Birth ◽  
Human Cervix ◽  
Ripening Of The Cervix

Proper cervical function is essential for a normal pregnancy and birth to occur. Understanding the mechanisms that take place in normal pregnancy will allow a better comprehension of the complications involved in premature cervical remodeling and lead to better methods of diagnostics and prevention for preterm birth. Unfortunately, human samples are not easily available, and samples that are collected are often confounded by variations in timing and region of cervix from which sample is collected. Animal models, specifically the mouse, have facilitated a great deal of exploration into the mechanisms of cervical function and pathways of preterm birth. This review highlights some of the groundbreaking discoveries that have arisen from murine research including 1) the identification of early pregnancy changes in collagen fibril processing and assembly that result in progressive modifications to collagen architecture with subsequent loss of tissue stiffness during pregnancy, 2) the determination that immune cells are not key to cervical ripening at term but have diverse phenotypes and functions inpostpartumrepair, and 3) the finding that the process of preterm cervical ripening can differ from term ripening and is dependent on the etiology of prematurity. These findings, which are relevant to human cervical biology, provide new insights that will allow targeted studies on the human cervix as well as identify potential biomarkers for early detection of premature cervical ripening and development of improved therapies to prevent premature ripening of the cervix and subsequent preterm birth.

scholarly journals Sheng-Di-Da-Huang Decoction Inhibited Inflammation Expressed in Microglia after Intracerebral Hemorrhage in Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Min Cai ◽  
Zhonghai Yu ◽  
Wen Zhang ◽  
Li Yang ◽  
Jun Xiang ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Water Content ◽  
Evans Blue ◽  
Microglial Activation ◽  
Critical Role ◽  
Neurological Deficits ◽  
Secondary Brain Injury ◽  
Brain Water Content ◽  
Evans Blue Extravasation ◽  
Brain Water

Objects. Sheng-Di-Da-Huang Decoction was used as an effective hemostatic agent in ancient China. However, its therapeutic mechanism is still not clear. Inflammatory injury plays a critical role in ICH-induced secondary brain injury. After hemolysis, hematoma components are released, inducing microglial activation via TLR4, which initiates the activation of transcription factors (such as NF-κB) to regulate expression of proinflammatory cytokine genes. This study aimed to verify the anti-inflammatory effects of Sheng-Di-Da-Huang Decoction on ICH rats. Materials and Methods. Intracerebral hemorrhage was induced by injection of bacterial collagenase (0.2 U) in rats. Neurological deficits, brain water content, Evans blue extravasation, expression of TLR4, NF-κB, Iba-1 positive cells (activated microglia), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) were examined 1, 3, 7, and 14 days after collagenase injection. MR images were also studied. Results. Sheng-Di-Da-Huang Decoction remarkably improved neurological function, reduced brain water content as well as Evans blue extravasation, downregulated expression of TLR4, NF-κB, TNF-α, and IL-1β, and inhibited microglial activation. Conclusions. Sheng-Di-Da-Huang Decoction reduced inflammation reaction after ICH through inhibited inflammation expressed in microglia.

scholarly journals Differential effects of spring reacclimation and deacclimation on cell membranes of Norway spruce seedlings

2013 ◽  
Vol 81 (4) ◽  
pp. 77-84 ◽  
Author(s):  
Paweł M. Pukacki ◽  
Emilia Kamińska-Rożek
Keyword(s):  
Low Temperature ◽  
Water Content ◽  
Norway Spruce ◽  
Freezing Tolerance ◽  
Cell Membranes ◽  
Total Phospholipid ◽  
Critical Role ◽  
Phospholipid Content ◽  
Temperature Exposure ◽  
Low Temperature Exposure

Two-year-old seedlings of Norway spruce (<em>Picea abies</em>) during spring deacclimation were subjected to controlled reacclimation by exposure to low temperatures of 4/−3°C (day/night) in a cold room. The highest increase in freezing tolerance (by 7°C) was observed after 12 d of low temperature exposure, when shoot water potential (Ψ<sub>w shoot</sub>) decreased to 0.64 MPa. The process of reacclimation was accompanied by an increase in the phospholipid content of needle cell membranes. This increase applied to total (PL) and individual phospholipids: phosphatidylcholine (PC), phosphatidylglycerol (PG), phosphatidylethanolamine (PE) and phosphatidic acid (PA). After being exposed to the low temperature for 18 d, the seedlings were moved into the open air. This caused deacclimation, with an increase in Ψ<sub>w shoot</sub> to −0.36 MPa and a decrease in the total phospholipid content and freezing tolerance of the needles. Significant correlations were observed between freezing tolerance, the membrane permeability (MP) of the needles and the phospholipid content, Ψ<sub>w shoot</sub> and water content of the needles. The results show that during spring deacclimation, Norway spruce seedlings can be subjected to reacclimation, which is reflected in the phospholipid content, the biophysical changes of the membranes, and the freezing tolerance of the seedlings. During both spring deacclimation and reacclimation, water content in the needles plays a critical role in the cold tolerance of spruce seedlings.

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