Lymphocyte Activity and the Role of Humoral Factors in Patients with Chronic Ocular Inflammation

Author(s):  
David BenEzra ◽  
Genia Maftzir
MicroRNA ◽  
2020 ◽  
Vol 09 ◽  
Author(s):  
Chrysanthos D. Christou ◽  
Georgios Tsoulfas

Introduction: Ischemia-reperfusion (I/R) injuries are caused by complex interrelated mechanisms and pathways. Regarding the liver, I/R injuries and their clinical manifestations are crucial for the surgical outcome. Despite its importance, there is no broadly accepted therapy either for the prevention or for the management of I/R injury. I/R injury of the liver can occur either during hepatic surgery (warm) or during the transplantation procedure (cold). MicroRNAs play a pivotal role in the mechanism of I/R injury, as they regulate the expression of the cellular participants and humoral factors associated with I/R injury. Objective: In this review, we highlight the microRNAs that are involved in the I/R injury of the liver, and the molecular pathways that they regulate. In addition, we discuss the potential role of circulating microRNAs as biomarkers and their role as pharmacological targets in the prevention, diagnosis and treatment of I/R injuries. Method: We conducted a comprehensive review of the PubMed bibliographic database regarding microRNAs and I/R injuries of the liver. Results: In diagnostics, microRNA panels could replace invasive diagnostic procedures, relieving patients of the associated complications. In therapeutics, microRNA agomirs, antagomirs and other drugs can be used to shift the balance between proapoptotic and survival pathways, to alleviate the liver damage caused by I/R. In transplantation procedures, microRNA profiling could decrease the incidence of early graft dysfunction, especially regarding marginal grafts. Conclusion: Although microRNAs seem a very promising clinical tool in the management of I/R injuries, further research is required, until microRNAs become a novel tool in the diagnosis and monitoring of an I/R injury of the liver.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Hyun-Jai Cho ◽  
Hyun-Ju Cho ◽  
Yoo-Wook Kwon ◽  
Young-Bae Park ◽  
Hyo-Soo Kim

Background: We recently identified bone marrow (BM)-derived artery resident calcifying progenitor cells. Sca-1+PDGFRα- cells may possess bipotent (osteoblastic/osteoclastic) characteristics. However, the nature of progenitor cells remains elusive. Hypothesis: We investigated developmental hierarchy of progenitor cells and in vivo dynamics in atherosclerosis. Methods and Results: We harvested cells from BM and artery of C57 mice. In BM, Lin-CD29+Sca-1+PDGFRα- cells showed hematopoietic potential and differentiated into osteoclasts (OC). They also possessed mesenchymal stem cell property including osteoblastic (OB) differentiation, suggesting that Sca-1+PDGFRα- cells could be mesodermal progenitor cells. Interestingly, BM-derived artery-resident, clonal Sca-1+PDGFRα- cells maintained bipotency but lost hematopoietic nature. In contrast, Sca-1+PDGFRα+ cells in BM and artery only showed unipotency (OB). When we overexpressed or knocked down PDGFRα, there was no alteration in OB or OC differentiation of Sca-1+PDGFRα- cells and no effect on OB differentiation of Sca-1+PDGFRα+ cells, indicating PDGFRα as a surface marker but not a functional player. In hyperlipidemic ApoE-KO mice compared with control, Sca-1+PDGFRα- cells were less mobilized from BM to peripheral circulation and less infiltrated into atherosclerotic plaque, whereas Sca-1+PDGFRα+ cells were not significantly affected. Multiplex cytokine assay of serum and artery revealed that IL-1β was significantly increased and IL-5 was markedly decreased in atherosclerotic mice. IL-1β decreased the migration of Sca-1+PDGFRα- cells by 5 folds compared with TNFα, and IL-5 increased the migration as much as TNFα. But the migration of Sca-1+PDGFRα+ cells was not altered. These data indicate that atherosclerosis-related humoral factors mainly regulated mesodermal progenitor cells’ dynamics. Conclusion: We demonstrate that Sca-1+PDGFRα- cell is a mesodermal progenitor cell that possesses both hematopoietic and mesenchymal potentials. In atherogenesis, the mobilization and infiltration of Sca-1+PDGFRα- progenitor cells were regulated by IL-1β and IL-5. These data provide a novel mechanism regarding the role of bipotent progenitor cells in atherosclerosis.


1937 ◽  
Vol 33 (4) ◽  
pp. 390-401
Author(s):  
L. S. Stern

At present, it can be considered indisputable that the coordination of body functions, based on the interaction of individual organs and physiological systems, is carried out simultaneously by nervous and humoral factors.


Physiology ◽  
1987 ◽  
Vol 2 (1) ◽  
pp. 22-26
Author(s):  
JA Schafer

Fluid absorption in the proximal tubule can be driven by a small osmotic difference between the luminal and interstitial fluids because this leaky epithelium has a high water permeability. The osmotic difference is produced by solute absorption, which tends to dilute the luminal fluid and concentrate the interstitial fluid. However, important questions remain unanswered regarding the pathway for water flow and the role of hemodynamic and humoral factors.


2012 ◽  
Vol 287 (15) ◽  
pp. 11616-11628 ◽  
Author(s):  
Ken-ichiro Tanaka ◽  
Erika Matsumoto ◽  
Yoshiko Higashimaki ◽  
Takenobu Katagiri ◽  
Toshitsugu Sugimoto ◽  
...  

The interaction between muscle tissues and bone metabolism is incompletely understood. We hypothesized that there might be some humoral factors that are produced in muscle tissues and exhibit bone anabolic activity. We, therefore, performed comparative DNA microarray analysis between mouse myoblastic C2C12 cells transfected with either stable empty vector or ALK2 (R206H), the mutation that constitutively activates the bone morphogenetic protein (BMP) receptor, to search for muscle-derived bone anabolic factors. Twenty-five genes whose expression was decreased to <1/4, were identified; these included osteoglycin (OGN). Stable overexpression of OGN significantly decreased the levels of Runx2 and Osterix mRNA compared with those in cells transfected with vector alone in MC3T3-E1 cells. On the other hand, it significantly enhanced the levels of alkaline phosphatase (ALP), type I collagen (Col1), and osteocalcin (OCN) mRNA as well as β-catenin and mineralization. A reduction in endogenous OGN level showed the opposite effects to those of OGN overexpression in MC3T3-E1 and mouse calvarial osteoblastic cells. Transient OGN overexpression significantly suppressed the levels of Runx2, Osterix, ALP, Col1, and OCN mRNA induced by BMP-2 in C2C12 cells. The conditioned medium from OGN-overexpressed and OGN-suppressed myoblastic cells enhanced and decreased, respectively, the levels of ALP, Col1, and β-catenin in MC3T3-E1 cells. Moreover, OGN increased Smad3/4-responsive transcriptional activity as well as Col1 mRNA levels independently of endogenous TGF-β in these cells. In conclusion, this study suggests that OGN may be a crucial humoral bone anabolic factor that is produced by muscle tissues.


1995 ◽  
Vol 116 (5) ◽  
pp. 2447-2450 ◽  
Author(s):  
Zun-Yi Wang ◽  
Rolf Håkanson

2008 ◽  
Vol 86 ◽  
pp. 0-0
Author(s):  
L CIMINO ◽  
M LOSI ◽  
L RICHELDI ◽  
L BOIARDI ◽  
L CAPPUCCINI ◽  
...  

Author(s):  
A. Fanchamps

SummaryThe classical vascular mechanism of migraine attacks demonstrated by Wolff — intracranial vasoconstriction during the prodromal stage and passive vasodilatation of extracranial arteries during the painful phase — has been confirmed by modern methods. Arterial distension is, however, not sufficient to explain the origin of the pain: to give rise to an acute migraineous pain, it must be associated with a lowered pain threshold of the receptors situated in the wall of the affected vessels. A number of humoral factors — plasmakinin, serotonin, histamine — intervene in the chain of events that culminates in migraine headache.At the start of the attack, the blood platelets release serotonin, the mast cells in the affected area release histamine and proteolytic enzymes that split plasmakininogens to form plas-makinins. Free serotonin and histamine increase capillary permeability and favor transudation of plasmakinin into the vessel walls andperivascular tissues. The combined effect of serotonin and plasmakinin on the vessel wall receptors reduces their pain threshold. On the other hand, the bulk of the released serotonin is excreted as 5-HIAA, and plasma serotonin falls. Since serotonin has a constricting effect on the extracranial arteries and a dilating one on the capillaries, the fall in its plasma level induces hypotonia of these arteries and capillary constriction, which results in a passive distension of the arterial walls. The two factors necessary for the production of pain are thus present: a low pain threshold and vascular distension. In addition to these three main humoral mediators, the part played by tyramine in migraine of alimentary origin, the precipitating effect of estrogen decrease in mentrual migraine and the hypothetical role of prostaglan-dins and prolactin are discussed.


Sign in / Sign up

Export Citation Format

Share Document