Attenuated expression of inducible nitric oxide synthase in lung microvascular endothelial cells is associated with an increase in ICAM-1 expression

Lo, Horace P.; Ackland-Berglund, Cathleen E.; Pritchard, Kirkwood A.; Guice, Karen S.; Oldham, Keith T.

doi:10.1053/jpsu.2001.25731

Cited by 19 publications

(9 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the adhesion of tumor cells to endothelium does not occur in the macrovascular circulation, but in the microvascular circulation 26. Microvascular endothelial cells react differently to stimuli compared to macrovascular endothelial cells 27, 28, 29, 30, 31, 32, 33. Furthermore, it is believed that endothelial cells from different organs have their own pattern of adhesion molecules 34, 35, 36, 37.…”

mentioning

confidence: 99%

Influence of proinflammatory cytokines on the adhesion of human colon carcinoma cells to lung microvascular endothelium

Kate

Hofland

Grevenstein

et al. 2004

Intl Journal of Cancer

View full text Add to dashboard Cite

Key words: proinflammatory cytokines; colon carcinoma; microvascular endothelium; adhesionLocoregional recurrence as well as recurrence to distant sites following intentionally curative surgery is a major problem in colorectal cancer. Recurrence rates up to 40% have been reported in colorectal cancer. 1 Among the sites of recurrences, the most frequent are liver, lung and locoregional sites. [2][3][4][5] Resection handling of the tumor can provoke detachment of tumor cells. Circulating tumor cells are often found in patients with gastrointestinal cancer, not only during resection of the primary tumor. 6 -8 Although the amount of circulating tumor cells is enhanced during resection of the primary tumor, it will not entirely explain the high recurrence rate found after intentionally curative surgery. Implantation of circulating tumor cells appears to be highly inefficient and most circulating tumor cells are rapidly destroyed. 9,10 It is possible that the surgical trauma itself influences the development of recurrences. Surgical peritoneal trauma provokes an inflammatory reaction, in which leukocytes are activated and cytokines and reactive oxygen species are released. We recently demonstrated that these factors enhance locoregional tumor recurrences. 11,12 However, these factors are released not only locally but also in the circulation. After major abdominal surgery, the proinflammatory cytokines interleukin-6 (IL-6), interleukin-1␤ (IL-1␤) and tumor necrosis factor-␣ (TNF-␣) in peripheral blood are elevated. [13][14][15][16][17] We hypothesize that these factors are not only involved in locoregional tumor recurrence after peritoneal trauma, but also in recurrences at distant sites.The lung is a frequent site for tumor recurrence in many gastrointestinal tumors. The process of hematogenous metastasis formation to the lung is a multistep event in which tumor cells first have to detach from the primary tumor, invade the bloodstream, subsequently adhere to the endothelium within the lung and finally invade and multiply to form lung metastases. 18,19 An important step in this process is the adhesion of tumor cells to the endothelium. It is known that the cytokines IL-1␤ and TNF-␣ enhance tumor cell adhesion to human umbilical venous endothelial cells (HUVECs) in vitro by upregulation of adhesion molecules on HUVECs. 20 -25 HUVECs are embryonic macrovascular cells used in many models studying the pathophysiology of the endothelium. However, the adhesion of tumor cells to endothelium does not occur in the macrovascular circulation, but in the microvascular circulation. 26 Microvascular endothelial cells react differently to stimuli compared to macrovascular endothelial cells. [27][28][29][30][31][32][33] Furthermore, it is believed that endothelial cells from different organs have their own pattern of adhesion molecules. 34 -37 Because of these differences, general extrapolation from data obtained from the HUVEC model to the microcirculation is most certainly invalid.We developed a reproducible human in vitro model...

show abstract

mentioning

confidence: 99%

Influence of proinflammatory cytokines on the adhesion of human colon carcinoma cells to lung microvascular endothelium

Kate

Hofland

Grevenstein

et al. 2004

Intl Journal of Cancer

View full text Add to dashboard Cite

show abstract

“…In physiological state, production of NO in lung is tightly regulated for short periods of time by two isoforms of constitutive nitric oxide synthases (NOS): endothelial NOS (eNOS) and neuronal NOS (nNOS) in airway epithelial cells pulmonary vascular endothelial cells, and noncholinergic, nonadrenergic nerve fibers [7]. However, in several pathological contexts, such as inflammation or endotoxininduced infection [8], a third isoform of inducible NOS (iNOS) is expressed and activated in several cells including neutrophils [9], macrophages [10], pulmonary microvascular endothelial cells [11] and pulmonary epithelial cells [12,13]. iNOS catalyzes subsequently over-production of inducible NO for prolonged period of time, which may mediate cellular and tissular damage.…”

Section: Introductionmentioning

confidence: 99%

Dexamethasone attenuated endotoxin-induced acute lung injury through inhibiting expression of inducible nitric oxide synthase

Zhang

Ouyang

2009

Clinical Hemorheology and Microcirculation

View full text Add to dashboard Cite

Application of glucocorticoids in sepsis or severe infection is disputable in clinic. In this experiment, we studied the effect of dexamethasone on nitric oxide synthases and whether dexamethasone could attenuate endotoxin-induced acute lung injury (ALI). SD rats received 5 mg/kg lipopolisaccharide (LPS) injection. Then arterial oxygen partial pressure (PaO 2 ), lung histology, lung tissue nitric oxide (NO) production and expression of nitric oxide synthases (NOS) were detected at 0.5, 1, 2, 3 or 4 h after LPS injection. PaO 2 and lung injury deteriorated upon time. Production of NO in lung tissue increased significantly particularly in the first two hours, and this change was mainly due to the over-expression of inducible NOS (iNOS), but not endothelial NOS (eNOS). Furthermore, a tight positive correlation was observed between lung injury score (LIS) and NO production level in lung tissue. Dexamethasone could ameliorate PaO 2 and lung damage evidently, which were paralleled by significant decreases in the production of NO and in the expression of iNOS mRNA. In conclusion, dexamethasone could effectively attenuate endotoxin-induced lung injury through inhibiting iNOS expression and activation in the very early stage of ALI.

show abstract

“…A number of studies have obviously established that testicular torsion produces severe destruction in spermatogenesis, and several enzymes and drugs have been used to prevent such injury in animal models and humans [2][3][4]. Damage to endothelial cells following ischemia-reperfusion (I/R) of other tissues such as cardiac and renal tissues after acute myocardial infarction or coronary artery disease, phases of ischemic acute renal failure and inflammatory diseases results in cell surface expression of cell adhesion molecules involved in PMN recruitment [5,6]. Cell-adhesion molecules, once believed to function primarily in tethering cells to extracellular ligands, are now documented as having broader functions in cellular signaling cascades [7].…”

Section: Introductionmentioning

confidence: 99%

The role of cell adhesion molecules in ischemic epididymal injury

Öztürk

Dokucu

2007

Int Urol Nephrol

View full text Add to dashboard Cite

show abstract

Attenuated expression of inducible nitric oxide synthase in lung microvascular endothelial cells is associated with an increase in ICAM-1 expression

Cited by 19 publications

References 19 publications

Influence of proinflammatory cytokines on the adhesion of human colon carcinoma cells to lung microvascular endothelium

Influence of proinflammatory cytokines on the adhesion of human colon carcinoma cells to lung microvascular endothelium

Dexamethasone attenuated endotoxin-induced acute lung injury through inhibiting expression of inducible nitric oxide synthase

The role of cell adhesion molecules in ischemic epididymal injury

Contact Info

Product

Resources

About