Post-transcriptional regulation of expression of plasminogen activator inhibitor type 1 mRNA by insulin and insulin-like growth factor 1.

Fattal, Peter; Schneider, David J.; Sobel, Burton E.; Billadello, Joseph J.

doi:10.1016/s0021-9258(18)42289-2

Cited by 94 publications

(7 citation statements)

References 49 publications

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“…Moreover, numerous studies revealed an abundant accumulation of growth factors and cytokines in keloids (Xue et al, 2000;Akimoto et al, 1999;Lee et al, 1999), some of which can be upregulated by hypoxia (Semenza, 2002). In addition to hypoxia, PAI-1 mRNA expression can be regulated by various growth factors, hormones, and cytokines under normoxic conditions (Sawdey and Loskuto¡, 1991;Fattal et al, 1992;Takeda et al, 2001). Most recently, studies have demonstrated that, in contrast to regulation via the ubiquitin proteasome pathway, certain translation regulatory proteins that are substrates of the PI3K-AKT-FRAP/mTOR cascade can be activated by a variety of growth factors and cytokines to induce HIF-1a accumulation and target gene expression (Stiehl et al, 2002;Semenza 2002;Huang and Bunn, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…PAI-1 can be synthesized and secreted by platelets (Erickson et al, 1985), vascular endothelial cells (Reilly and McFall, 1991), vascular smooth muscle cells (Reilly and McFall, 1991), and several nonvascular cell types (Busso et al, 1994). PAI-1 gene expression can be regulated by a variety of stimuli, including phorbol ester (Descheemaeker et al, 1992), transforming growth factor-b (Sawdey and Loskuto¡, 1991;Song et al, 1998), tumor necrosis factor-a (Sawdey and Los-kuto¡, 1991), interleukin-1 (Bevilacqua et al, 1986), lipopolysaccharide (Crutchley and Conanan, 1986;Sawdey and Loskuto¡, 1991), insulin, and insulin like growth factor-1 (Fattal et al, 1992;Ban¢ et al, 2001), platelet-derived growth factor (Reilly and McFall, 1991), and angiotensin II (Feener et al, 1995;Takeda et al, 2001). Recent studies reported an upregulation of PAI-1 gene expression induced by low oxygen tension (hypoxia) in trophoblast cells (Fitzpatrick and Graham, 1998), hepatocytes (Kietzmann et al, 1999), endothelial cells (Uchiyama et al, 2000), transformed murine macrophages (Pinsky et al, 1998), and some cancer cell lines (Fink et al, 2001).…”

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confidence: 99%

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Mechanisms of Hypoxic Regulation of Plasminogen Activator Inhibitor-1 Gene Expression in Keloid Fibroblasts

Zhang

Ann

et al. 2003

Journal of Investigative Dermatology

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Keloids are an excessive accumulation of extracellular matrix. Although numerous studies have shown elevated plasminogen activator inhibitor-1 (PAI-1) levels in keloid fibroblasts compared with those of normal skin. Their specific mechanisms involved in the differential expression of PAI-1 in these cell types. In this study, the upregulation of PAI-1 expression is demonstrated in keloid tissues and their derived dermal fibroblasts, attesting to the persistence, if any, of fundamental differences between in vivo and in vitro paradigms. We further examined the mechanisms involved in hypoxia-induced regulation of PAI-1 gene in dermal fibroblast derived from keloid lesions and associated clinically normal peripheral skins from the same patient. Primary cultures were exposed to an environmental hypoxia or desferroxamine. We found that the hypoxia-induced elevation of PAI-1 gene appears to be regulated at both transcriptional and post-transcriptional levels in keloid fibroblasts. Furthermore, our results showed a consistent elevation of HIF-1alpha protein level in keloid tissues compared with their normal peripheral skin controls, implying a potential role as a biomarker for local skin hypoxia. Treatment with antisense oligonucleotides against hypoxia-inducible factor 1alpha (HIF-1alpha) led to the downregulation of steady-state levels of PAI-1 mRNA under both normoxic and hypoxic conditions. Conceivably, our results suggest that HIF-1alpha may be a novel therapeutic target to modulate the scar fibrosis process.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Mechanisms of Hypoxic Regulation of Plasminogen Activator Inhibitor-1 Gene Expression in Keloid Fibroblasts

Zhang

Ann

et al. 2003

Journal of Investigative Dermatology

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“…In rodents, the increase in plasmin and PA activities triggered by unilateral teat sealing or litter removal was inhibited by PRL (Tonner et al, 2000). It has been suggested that PRL enhances PAI-1 release by inhibiting IGFBP-5 synthesis, thus leading to tPA inactivation (Fattal et al, 1992;Tonner et al, 2000). Moreover, the decreases in mammary gland weight and DNA content and the increase in PA concentration that are naturally observed during involution were all reduced by injections of PRL in mice (Ossowski et al, 1979).…”

Section: Prl Inhibition As a Tool To Accelerate Mammary Gland Involutionmentioning

confidence: 98%

Invited review: Accelerating mammary gland involution after drying-off in dairy cattle

Zhao

Ponchon

Lanctôt

et al. 2019

Journal of Dairy Science

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Bovine mammary gland involution, as a part of the reproductive cycle in dairy cows, is a very important remodeling transformation of the mammary gland for the subsequent lactation. There is considerable incentive to accelerate mammary gland involution to improve udder health, shorten the dry period, and simplify the management process by reducing dietary changes. The complex process of mammary involution is characterized by morphological changes in the epithelial cells and mammary tissue, changes in the composition of mammary secretions, and changes in the integrity of tight junctions. Involution is facilitated by elements of the immune system and several types of proteases and is coordinated by various types of hormones. This review first describes the involution process and then argues for the need to accelerate it. Last, this review focuses on various intervention methods for accelerating involution. Our aim is to provide a comprehensive overview of bovine mammary gland involution as well as potential techniques and new opinions for dry cow management.

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“…Atheroma from coronary arteries harvested by atherectomy from patients with type 2 diabetes and compared with those from nondiabetic age and gender matched subjects exhibit markedly increased concentrations of PAI-1 and markedly diminished concentrations of plasminogen activators (28). Mechanisms responsible for induction of PAI-1 synthesis by insulin appear to include stabilization of PAI-1 mRNA (29). Thus, insulin prolongs the half life of the 3.2-kb PAI-1 mRNA species by 2.7-fold in Hep G2 cells exposed to concentrations of insulin comparable to those encountered in association with diabetes.…”

Section: Impaired Fibrinolysis With Diabetesmentioning

confidence: 99%

Fibrinolysis and diabetes

Sobel¹

2003

Front Biosci

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Diabetes is characterized by impaired fibrinolysis. This phenomenon reflects augmented concentrations of plasminogen activator inhibitor type-1 in tissues and in blood. The derangement appears to depend in part on elevated concentrations of free fatty acids, triglycerides, and insulin in association with the insulin resistance syndrome. Impaired fibrinolysis may exacerbate already existing coronary artery disease and potentiate its evolution. Several measures are available to favorably modify fibrinolytic system capacity. They include inhibition of the renin angiotensin system, attenuation of dyslipidemia, and enhancement of insulin sensitivity. Accordingly, normalization of the derangement in fibrinolysis typical of diabetes is an important and achievable therapeutic objective.

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Post-transcriptional regulation of expression of plasminogen activator inhibitor type 1 mRNA by insulin and insulin-like growth factor 1.

Cited by 94 publications

References 49 publications

Mechanisms of Hypoxic Regulation of Plasminogen Activator Inhibitor-1 Gene Expression in Keloid Fibroblasts

Mechanisms of Hypoxic Regulation of Plasminogen Activator Inhibitor-1 Gene Expression in Keloid Fibroblasts

Invited review: Accelerating mammary gland involution after drying-off in dairy cattle

Fibrinolysis and diabetes

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