Effects of 1,25-Dihydroxy vitamin D3 on TNF-α induced inflammation in human chondrocytes and SW1353 cells: a possible role for toll-like receptors

Avcıoğlu, Gamze; İpteç, Betül Özbek; Akcan, Gülben; Görgün, Büşra; Fidan, Kübra; Çarhan, Ahmet; Yılmaz, Gülsen; Kozacı, Didem

doi:10.1007/s11010-019-03655-z

Cited by 9 publications

(6 citation statements)

References 38 publications

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“…D reduced inflammatory responses in both endothelial cells and db/db mice exposed to a diabetes-like environment (Einbinder et al 2016 ). The addition of 1,25-dihydroxyvitamin D 3 reduced TNF-α-induced inflammation in human chondrocytes (Avcioglu et al 2020 ). In this study, TNF-α treatment increased tumor necrosis factor receptor-2 (TNFR2) expression in A549 cells, while Vit.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D3 decreases TNF-α-induced inflammation in lung epithelial cells through a reduction in mitochondrial fission and mitophagy

et al. 2021

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and mechanisms of action of vitamin D 3 (Vit. D) on the expression of intercellular adhesion molecule-1 (ICAM-1) in vitro and in vivo with or without tumor necrosis factor α (TNF-α) treatment. Pretreatment with Vit. D reduced the expression of ICAM-1 and leukocyte adhesion in TNF-α-treated A549 cells. TNF-α increased the accumulation of mitochondrial reactive oxygen species (mtROS), while Vit. D reduced this effect. Pretreatment with Vit. D attenuated TNF-α-induced mitochondrial fission, as shown Abstract Previous work has shown an association between vitamin D 3 deficiency and an increased risk for acquiring various inflammatory diseases. Vitamin D 3 can reduce morbidity and mortality in these patients via different mechanisms. Lung inflammation is an important event in the initiation and development of respiratory disorders. However, the anti-inflammatory effects of vitamin D 3 and the underlying mechanisms remained to be determined. The purpose of this study was to examine the effects

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Section: Discussionmentioning

confidence: 99%

Vitamin D3 decreases TNF-α-induced inflammation in lung epithelial cells through a reduction in mitochondrial fission and mitophagy

et al. 2021

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“…The murine model also showed that 1,25(OH)2D3 controlled chondrocyte proliferation and differentiation directly 29 . We suspected that calcitriol may maintain the normal proliferation of articular chondrocytes by accelerating chondrocyte apoptosis 13,14,29 in patients with PPRD. Therefore, our preliminary data with five patients for more than one year suggest that calcitriol may provide a potential treatment option for PPRD patients with vitamin D deficiency.…”

Section: Discussionmentioning

confidence: 99%

“…1,25(OH)2D3 (calcitriol), which is used to treat hypocalcemia, osteoporosis, and prevention of corticosteroid-induced osteoporosis 12 . It accelerates chondrocyte apoptosis and improve physical function in rats with RA by the inhibition of NF-κB signal pathway 13 and showed chondroprotective effects in human chondrocytes 14 . We suspected that calcitriol may maintain the normal proliferation of articular chondrocytes by accelerating chondrocyte apoptosis.…”

Section: Introductionmentioning

confidence: 99%

A retrospective study of nine patients with progressive pseudorheumatoid dysplasia: to explore early diagnosis and further treatment

et al. 2021

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Background: Most patients with progressive pseudorheumatoid dysplasia (PPRD) are initially misdiagnosed because of disease rarity and lack of awareness by most clinicians. The purpose of this present study was to provide further early diagnostic options and potential treatment to patients with PPRD. Methods: This was a retrospective study. Clinical manifestations, laboratory test results, radiographic features, Sanger Sequencing to determine CCN6 gene variants, treatment and follow-up records were collected in the patients with PPRD. Time to diagnosis, phenotype and genotype correlation were analyzed. Results: Nine PPRD children were included. There were 3 pairs of siblings and one patient had parental consanguinity. Five patients were misdiagnosed as juvenile idiopathic arthritis (JIA). The onset of disease in 8 patients was between 3 to 6 years of age. The interval from onset of symptoms to obtaining the diagnosis for 8 of the patients varied from 3.6 years to 20 years. The onset of symptoms included enlarged and stiff interphalangeal joints of the fingers, gait disturbance or joint pain. Laboratory tests revealed normal range of inflammatory parameters. Serum levels of 25-hydroxyvitamin D3 in six patients were below the normal range. Radiographic findings included different degree of abnormal vertebral bodies, epiphyseal enlargement of the interphalangeal joints with juxta-articular osteopenia, or cyst-like structures femoral head. All the patients harbored CCN6 variants, and a total of 7 variants were identified. After the treatment of calcitriol in 5 patients with low level of 25-hydroxyvitamin D3 for 1.25 years to 1.75 years, two of them kept stable, while 3 of them improved gradually. Conclusions: Combining the patient's family history, clinical features presenting with abnormal gait or enlarged and stiff interphalangeal joints of the fingers, normal inflammatory markers, and the characteristic radiographic findings, we can obtain the clinical diagnosis of PPRD for the patients at a very early stage of the disease. Anterior blunt of the vertebral bodies could be an early radiological sign in the patient even without obvious clinical symptoms and characteristics yet. The patients with PPRD having c.624dupA variant in CCN6 may have delayed onset. Underlying vitamin D deficiency should be sought and corrected in patients with PPRD.

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“…Concerning their normal liver function, serum creatinine, serum calcium, phosphate, alkaline phosphatase, parathyroid hormone, we treated our patients that presented with low serum level of 25-hydroxyvitamin D3 with oral calcitriol and in the follow-up appointment found that 2/6 patient's symptoms stopped progressing, while 4/6 patient's symptoms improved gradually. We suspected that calcitriol may maintain the normal proliferation of articular chondrocytes by accelerating chondrocyte apoptosis [11][12][13] in patients with PPRD. Therefore, our preliminary data with six patients suggest that calcitriol may provide a new beneficial treatment option for PPRD.…”

Section: Discussionmentioning

confidence: 99%

“…1,25(OH)2D3 (calcitriol), which is used to treat hypocalcemia, osteoporosis, and prevention of corticosteroid-induced osteoporosis 10 , has showed chondro-protective effects in human chondrocytes 11 . Combined with the results of a murine model to study the role of 1,25(OH)2D3, the patients and rat model with rheumatoid arthritis, and the properties of patient's cartilage and chondrocytes under PPRD, we suspected that calcitriol may maintain the normal proliferation of articular chondrocytes by accelerating chondrocyte apoptosis [12][13][14] and could thus be used to treat PPRD.…”

Section: Introductionmentioning

confidence: 99%

Systematical analysis of nine Chinese patients with progressive pseudorheumatoid dysplasia and assessment of calcitriol treatment

Li¹,

Mao²,

Zhou³

et al. 2020

Preprint

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Background: Progressive pseudorheumatoid dysplasia (PPRD) (MIM 208230) is a rare genetic disease characterized by progressive noninflammatory arthropathy affecting primarily the articular cartilage. Most patients are initially misdiagnosed because of the rarity of the disease and lack of awareness by most clinicians. Therefore, the purpose of the present study was to provide further diagnostic options to help clinicians make early precise diagnosis, and to investigate a new potential treatment for patients with PPRD. Methods: Clinical manifestations, radiographic features, Sanger Sequencing to determine WISP3 gene mutation and follow-up records were collected in 9 Chinese patients with PPRD. The time until diagnosis, relationship between clinical phenotypes and genotypes, and treatment effects were analyzed. Results: The clinical history and characteristics, mutations in the WISP3 gene, radiological data, treatment and outcome of 9 PPRD children were collected and reviewed. There were 3 pairs of siblings in this group and one patient had parental consanguinity. Five patients were misdiagnosed with juvenile idiopathic arthritis (JIA). The onset of disease in most patients (8/9) was between 3 and 6 years of age. The interval between onset of symptoms and obtaining the diagnosis for 8 of the patients varied between 3.6 years to 20 years. The onset of symptoms included enlarged and stiff interphalangeal joints of the fingers, gait disturbance or joint pain. Blood analysis revealed normal range of inflammatory parameters (erythrocyte sedimentation rate, C-reactive protein). Serum levels of 25-hydroxyvitamin D3 were analyzed in six patients and ranged from 6.16 to 22.1ng/ml, all lower than the normal range. Radiographic findings included different degree of abnormal vertebral bodies, epiphyseal enlargement of the interphalangeal joints with juxta-articular osteopenia, or reduction in hip articular space and cyst-like structures femoral head. A total of 7 variants in the WISP3 gene were identified in the 9 cases, presenting with three homozygous variants (c.397_404delCAAGTGTT, c.667T>G, and c.589+2T>C) and three compound heterozygous variants (c.589+2T>C/c.667T>G, c.624dupA/c.756C>A, and c.646T>C/c.1000T>C). After the treatment of calcitriol in the 6 patients with low level of 25-hydroxyvitamin D3 for 1.25 years to 1.75 years, two cases showed stable clinical disease activity and the other four patients joints’ pain and abnormal gait had improved. Conclusions: Combining the patient’s family history, clinical features presenting with abnormal gait or enlarged and stiff interphalangeal joints of the fingers, normal inflammatory markers, and the characteristic radiographic findings, we can obtain the clinical diagnosis of PPRD for the patients at a very early stage of the disease. The patients with PPRD having c.624dupA mutation in WISP3 may have delayed onset. Calcitriol showed treatment benefit by improving symptoms and decelerating progression of PPRD disease.

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Effects of 1,25-Dihydroxy vitamin D3 on TNF-α induced inflammation in human chondrocytes and SW1353 cells: a possible role for toll-like receptors

Cited by 9 publications

References 38 publications

Vitamin D3 decreases TNF-α-induced inflammation in lung epithelial cells through a reduction in mitochondrial fission and mitophagy

Vitamin D3 decreases TNF-α-induced inflammation in lung epithelial cells through a reduction in mitochondrial fission and mitophagy

A retrospective study of nine patients with progressive pseudorheumatoid dysplasia: to explore early diagnosis and further treatment

Systematical analysis of nine Chinese patients with progressive pseudorheumatoid dysplasia and assessment of calcitriol treatment

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