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Vocal cord nodules

Vocal cord nodules sorry, can

Noteworthy, both spare respiratory capacity and glycolytic capacity were significantly lower after instant nifedipine treatment, as compared to the 24 h application suggesting that those parameters respond immediately and then gradually are compensated.

Conversely, only long nifedipine treatment augmented glycolytic reserve, suggesting an efficient switch to compensatory energetic production in chondrocytes. BMMSCs responded differently: only long (24 h) application downregulated basal respiration level and ATP production, whereas no induction of glycolysis was observed.

Altogether these data suggest that nifedipine may lead to an energetic arrest in BMMSCs and chondrocytes, which could also, at least in vocal cord nodules, account for the reduced proliferation, as was shown in the study with berberine in HepG2, HeLa, species Hepa1-6 cell lines (30).

In agreement to that, the analysis of chondrocyte vocal cord nodules by electron microscopy in cartilage explant histological sections has also suggested that part of mitochondria lose their activity in response to nifedipine. Unexpectedly, the VOCC agonist BayK8644 had similar metabolic effects to nifedipine, including induction of glycolytic reserve in chondrocytes and blockage of ATP production in both chondrocytes and BMMSC.

Intracellular calcium levels were huntington decreased, but unexpectedly increased in nifedipine, while not BayK8644 treated cells of both types.

These data are in agreement to the previously observed upregulation of intracellular calcium by vocal cord nodules from ryanodine receptor-mediated endoplasmic reticulum stores of neonatal neuromuscular junction in rats, suggesting a compensatory mechanism in cells (32).

Furthermore, similar increase in intracellular calcium was also determined in porcine aortic endothelial cells that do not express L-type calcium channels (34), suggesting potential involvement of additional mechanisms of nifedipine action in different cell types.

Nifedipine has been shown to increase endothelial NO bioavailability (13), and upregulating intracellular calcium in striatal neurons (35), whereas inhibition of mitochondrial activity by NO has been demonstrated (36). Similarly, in the present study, NO activity was stimulated by nifedipine in BMMSCs and particularly chondrocytes, suggesting that NO at least in part may account for the effects of nifedipine on metabolism in both tested cell types.

Conversely, BayK8644 had no effect on NO activity, although it was the most potent blocker of ATP in chondrocytes, suggesting that vocal cord nodules mechanisms might be implicated in its action on mitochondrial respiration. Finally, the effects of nifedipine and BayK8644 on chondrogenesis and extracellular matrix production were assessed in chondrocytes and BMMSCs. Taken together, we conclude that the antihypertensive drug nifedipine inhibits mitochondrial respiration in both chondrocytes and BMMSCs, and that these effects may be associated with the increased NO production and pro-inflammatory activity.

Glycolytic capacity was enhanced only in chondrocytes, suggesting that these cells have the capacity to switch from oxidative phosphorylation to glycolysis and alter their metabolic activity in response to VOCC inhibition. Finally, nifedipine had positive effects on the production of collagen type II and proteoglycans in both cell types, implying potentially beneficial anabolic responses in articular cartilage. These results highlight a potential link between antihypertensive drugs and cellular changes that occur in chondrocytes in OA cartilage.

The data that support the findings of this study are available from the corresponding author, EB, upon reasonable request. The studies involving human participants were reviewed and approved by Vilnius Regional Committee on Biomedical Research Vocal cord nodules. IU, EBe, GR, EBa, and JD: writing-original draft preparation.

GK and NP: patient selection, tissue sample preparation, and manuscript editing. EBe: study design and supervision. AM: conceptualization, mens masturbation of metabolic studies, and manuscript editing. ZM: transmission electron microscopy study, histological analysis of chondrogenic differentiation pellet samples. The Innovative Medicines Initiative Joint Women sperm under grant agreement No.

We would like to thank Dr. Irute Girkontaite for her help during calcium measurements, Romute Griniene for histological analysis support and Saule Valiuniene for cell culture technical support.

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