Experimental research Effect of 1α-25-dihydroxyvitamin D 3 on intimal hyperplasia developing in vascular anastomoses: a rabbit model

Yurekli, Ismail; Gokalp, Orhan; Kıray, Müge; Bademci, Mehmet Şenel; Yetkin, Ufuk; Ergunes, Kazim; Yılmaz, Osman; Bayrak, Serdar; Gürbüz, Ali

doi:10.5114/aoms.2012.30786

Cited by 4 publications

(5 citation statements)

References 15 publications

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“…There were no statistically significant differences between the vehicle and paricalcitol arteries. However, trends in stenosis were observed that were generally aligned with data published in the literature [10,20]. Next, we explored potential mediators of tissue injury in intimal hyperplasia secondary to endothelial damage and the effect of paricalcitol.…”

Section: Paricalcitol Intimal Hyperplasia and Stenosis Secondary To E...supporting

confidence: 66%

“…Vitamin D had previously been reported to protect from neointimal hyperplasia [10,11,20,21], although not by all authors [22]. However, the therapeutic use of vitamin D is marred by potential adverse effects on calcium-phosphate metabolism, as overdosing can cause hypercalcemia, hyperphosphatemia, hypercalciuria, urolithiasis, nephrocalcinosis and kidney failure [29][30][31][32].…”

Section: Discussionmentioning

confidence: 99%

“…Sci. 2024, 25, 4814 2 of 15 (EGF) and elastin gene expression [6,8,9], all of which may reduce the development of intimal hyperplasia in vivo following vascular injury [10,11].…”

Section: Introductionmentioning

confidence: 99%

“…Given that vitamin D had previously been reported to protect from neointimal hyperplasia [10,11,20,21], although not by all authors [22], and that the neointima is rich in VDR [23], we studied the impact of paricalcitol on neointimal hyperplasia and potential molecular targets in rats. The information obtained may identify novel therapeutic targets for human disease.…”

Section: Introductionmentioning

confidence: 99%

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Paricalcitol Has a Potent Anti-Inflammatory Effect in Rat Endothelial Denudation-Induced Intimal Hyperplasia

Baeza,

Pintor-Chocano,

Carrasco

et al. 2024

IJMS

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Neointimal hyperplasia is the main cause of vascular graft failure in the medium term. Vitamin D receptor activation modulates the biology of vascular smooth muscle cells and has been reported to protect from neointimal hyperplasia following endothelial injury. However, the molecular mechanisms are poorly understood. We have now explored the impact of the selective vitamin D receptor activator, paricalcitol, on neointimal hyperplasia, following guidewire-induced endothelial cell injury in rats, and we have assessed the impact of paricalcitol or vehicle on the expression of key cell stress factors. Guidewire-induced endothelial cell injury caused neointimal hyperplasia and luminal stenosis and upregulated the expression of the growth factor growth/differentiation factor-15 (GDF-15), the cytokine receptor CD74, NFκB-inducing kinase (NIK, an upstream regulator of the proinflammatory transcription factor NFκB) and the chemokine monocyte chemoattractant protein-1 (MCP-1/CCL2). Immunohistochemistry confirmed the increased expression of the cellular proteins CD74 and NIK. Paricalcitol (administered in doses of 750 ng/kg of body weight, every other day) had a non-significant impact on neointimal hyperplasia and luminal stenosis. However, it significantly decreased GDF-15, CD74, NIK and MCP-1/CCL2 mRNA expression, which in paricalcitol-injured arteries remained within the levels found in control vehicle sham arteries. In conclusion, paricalcitol had a dramatic effect, suppressing the stress response to guidewire-induced endothelial cell injury, despite a limited impact on neointimal hyperplasia and luminal stenosis. This observation identifies novel molecular targets of paricalcitol in the vascular system, whose differential expression cannot be justified as a consequence of improved tissue injury.

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Section: Paricalcitol Intimal Hyperplasia and Stenosis Secondary To E...supporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

“…Sci. 2024, 25, 4814 2 of 15 (EGF) and elastin gene expression [6,8,9], all of which may reduce the development of intimal hyperplasia in vivo following vascular injury [10,11].…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Paricalcitol Has a Potent Anti-Inflammatory Effect in Rat Endothelial Denudation-Induced Intimal Hyperplasia

Baeza,

Pintor-Chocano,

Carrasco

et al. 2024

IJMS

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“…An antiproliferative effect of 1α-25-dihydroxyvitamin D 3 on smooth muscle cells was recently studied. Hyperplasia developing in vascular anastomoses was significantly lowered [ 11 ]. That finding may be important because vitamin D 3 deficit is a common finding in hemodialysed patients.…”

Section: Discussionmentioning

confidence: 99%

Use of short prosthesis segments for brachiocephalic arteriovenous fistulas in elderly hemodialysis population

Głowiński

Małyszko

Głowińska

et al. 2014

aoms

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IntroductionThe autogenous brachiocephalic fistula is a recognized secondary access for hemodialysis. However, veins in the antecubital fossa are often damaged, due to repeated venipunctures and subsequent scarring. Sometimes their anatomy does not enable successful arteriovenous fistula creation. In cases when the proximal part of the cephalic vein seemed patent, during ultrasound Doppler examination, we decided to use a short segment of 6 mm polytetrafluoroethylene graft to connect the vein with the brachial artery. We report our series of this procedure.Material and methodsOver an 8-year period, 34 patients underwent such an operation. Grafts were anastomosed either to the end of the cephalic vein or to the side. The decision was made based on the vein condition: small-caliber veins were considered better for the end-to-side anastomosis. All procedures were performed under local anesthesia, and were well tolerated.ResultsThirty-three fistulas were successfully cannulated at 2-8 weeks after the operation. Fistula patency rates were 84%, 73% and 55% at 12, 24 and 36 months. Comparison of two anastomosis types showed differences, 50% and 62.8% at 36 months, yet without statistical significance (p = 0.27, log-rank test). Fistula patency was not influenced by patient's age, sex or comorbidities.ConclusionsThe described procedure provides satisfactory cumulative patency with an acceptable complication rate. It can enhance the number of cephalic veins used with its main advantages of simple surgical technique and low perioperative morbidity.

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1,25-Dihydroxyvitamin D3 attenuates disease severity and induces synoviocyte apoptosis in a concentration-dependent manner in rats with adjuvant-induced arthritis by inactivating the NF-κB signaling pathway

et al. 2018

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An aggressive proliferation of synoviocytes is the hallmark of rheumatoid arthritis (RA). Emerging evidence shows that inhibiting the NF-κB signaling pathway with 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] may be a therapeutic approach for controlling inflammatory diseases. In this study, we demonstrated the protective effects of three different 1,25(OH)2D3 concentration on adjuvant-induced arthritis (AA) rats through the NF-κB signaling pathway and their pro-apoptotic roles in cultured adjuvant-induced arthritis synoviocytes (AIASs). AA rats were prepared by injecting complete Freund's adjuvant and independently given daily intraperitoneal injection of 1,25(OH)2D3 at concentrations of 50, 100, and 300 ng/day/kg. Subsequently, AIASs were isolated from the inflamed joints of AA rats to test the effects of 1,25(OH)2D3 on AIASs in vitro. Intraperitoneal injection of 1,25-(OH)2D3 was found to induce a concentration- and time-dependent improvement in relieving the symptoms of AA. We found an increased paw withdrawal thermal latency (PWTL) in the affected paw of AA rats as the concentration of 1,25-(OH)2D3 increased. 1,25-(OH)2D3 treatment reduced levels of inflammatory factors in synovial tissues of AA rats. In the case of cultured AIASs, 1,25-(OH)2D3 was shown to inhibit cell proliferation and induce cell apoptosis in a concentration-dependent manner. Additionally, 1,25-(OH)2D3 inhibited the activation of the NF-κB signaling pathway. In conclusion, our study provides evidence emphasizing that 1,25(OH)2D3 has the potential to attenuate disease severity in RA potentially due to its contributory role in synoviocyte proliferation and apoptosis. The protective role of 1,25(OH)2D3 against RA depends on the NF-κB signaling pathway.

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Experimental research Effect of 1α-25-dihydroxyvitamin D 3 on intimal hyperplasia developing in vascular anastomoses: a rabbit model

Cited by 4 publications

References 15 publications

Paricalcitol Has a Potent Anti-Inflammatory Effect in Rat Endothelial Denudation-Induced Intimal Hyperplasia

Paricalcitol Has a Potent Anti-Inflammatory Effect in Rat Endothelial Denudation-Induced Intimal Hyperplasia

Use of short prosthesis segments for brachiocephalic arteriovenous fistulas in elderly hemodialysis population

1,25-Dihydroxyvitamin D3 attenuates disease severity and induces synoviocyte apoptosis in a concentration-dependent manner in rats with adjuvant-induced arthritis by inactivating the NF-κB signaling pathway

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