Isolation and Characterization of Cardiac Mesenchymal Stromal Cells from Endomyocardial Bioptic Samples of Arrhythmogenic Cardiomyopathy Patients

Pilato, Chiara Assunta; Stadiotti, Ilaria; Maione, Angela Serena; Saverio, Valentina; Catto, Valentina; Tundo, Fabrizio; Russo, Antonio Dello; Tondo, Claudio; Pompilio, Giulio; Casella, Michela; Sommariva, Elena

doi:10.3791/57263-v

Cited by 2 publications

(4 citation statements)

References 13 publications

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“…Based on the fact, the lipid metabolism plays a pivotal role in osteoporosis development. In the previous study, many factors had been revealed to involve in the balance of osteogenesis and adipogenesis including hypoxia, immune disturbance, and biological rhythm 27–29 . Additionally, there were some problems with lipid metabolism among the high‐risk groups of osteoporosis such as postmenopausal osteoporosis and diabetes patients 30,31 .…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Trehalose improves palmitic acid‐induced apoptosis of osteoblasts by regulating SIRT3‐medicated autophagy via the AMPK/mTOR/ULK1 pathway

et al. 2022

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Accumulation of lipid substances decreased the activity of osteoblasts. Trehalose is a typical stress metabolite to form a protective membrane on cell surface which has been demonstrated to regulate lipid metabolism. This activity of Trehalose indicates the potential effect of osteoporosis treatment. Our study aimed to determine the therapeutic effect of Trehalose in high fat-induced osteoporosis. We used palmitic acid (PA) to mimic the state of high fat and observed the apoptosis ratio of osteoblasts increased. After adding Trehalose, the apoptosis ratio decreased obviously. Autophagy is a regulatory means involved in the process of apoptosis.We detected the autophagy protein and found that the expression of Beclin-1, Atg5, and LC3 II increased, and p62 decreased after Trehalose treatment. When adding an autophagy inhibitor (3-MA), the expression of Beclin-1, Atg5, and LC3 II decreased, and p62 increased. These results indicated autophagy was an important factor involved in the preventive effect of Trehalose in PA-induced apoptosis. SIRT3 is a mitochondrial gene that can inhibit apoptosis, which has been reported to promote autophagy. We used SIRT3-siRNA to silence the expression of SIRT3 and found the effect of Trehalose was counteracted. The apoptosis ratio increased and the expression of Beclin-1, Atg5, and LC3 II decreased, p62 increased. Additionally, we also fed the mice with a high-fat diet (HFD) and intragastrical Trehalose. The results showed that Trehalose could inhibit the bone mass loss with HFD. Our study revealed the effect and mechanism of Trehalose in the treatment of osteoporosis.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: Trehalose improves palmitic acid‐induced apoptosis of osteoblasts by regulating SIRT3‐medicated autophagy via the AMPK/mTOR/ULK1 pathway

et al. 2022

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“…To confirm that defective PKP2 in sadipose tissue is mostly associated with gene expression patterns suggestive of impaired fat cell cycle, we took advantage of subcutaneous adipose tissues collected in a heterozygous ( Pkp2 +/− ) Pkp2 knockout mouse model 2 , 53 (Fig. 5a ), and analysed the subcutaneous stromal cells obtained from fat biopsy sampling in PKP2 -dependent arrhythmogenic cardiomyopathy (ACM) patients (Table S5 ) 17 , 54 , as illustrated in Fig. 5b .…”

Section: Resultsmentioning

confidence: 99%

“…Human subcutaneous fat-derived stromal cells were isolated as previously described in ref. 54 . Briefly, bioptic samples were washed with PBS, minced using sterile scissors, and incubated in IMDM (Invitrogen, #21980-032) containing 3 mg/ml collagenase NB4 (Serva, DS17454) at 37 °C for 1.5 h under continuous agitation.…”

Section: Methodsmentioning

confidence: 99%

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Impaired Plakophilin-2 in obesity breaks cell cycle dynamics to breed adipocyte senescence

Lluch,

Latorre,

Serena-Maione

et al. 2023

Nat Commun

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Plakophilin-2 (PKP2) is a key component of desmosomes, which, when defective, is known to promote the fibro-fatty infiltration of heart muscle. Less attention has been given to its role in adipose tissue. We report here that levels of PKP2 steadily increase during fat cell differentiation, and are compromised if adipocytes are exposed to a pro-inflammatory milieu. Accordingly, expression of PKP2 in subcutaneous adipose tissue diminishes in patients with obesity, and normalizes upon mild-to-intense weight loss. We further show defective PKP2 in adipocytes to break cell cycle dynamics and yield premature senescence, a key rheostat for stress-induced adipose tissue dysfunction. Conversely, restoring PKP2 in inflamed adipocytes rewires E2F signaling towards the re-activation of cell cycle and decreased senescence. Our findings connect the expression of PKP2 in fat cells to the physiopathology of obesity, as well as uncover a previously unknown defect in cell cycle and adipocyte senescence due to impaired PKP2.

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Isolation and Characterization of Cardiac Mesenchymal Stromal Cells from Endomyocardial Bioptic Samples of Arrhythmogenic Cardiomyopathy Patients

Cited by 2 publications

References 13 publications

RETRACTED: Trehalose improves palmitic acid‐induced apoptosis of osteoblasts by regulating SIRT3‐medicated autophagy via the AMPK/mTOR/ULK1 pathway

RETRACTED: Trehalose improves palmitic acid‐induced apoptosis of osteoblasts by regulating SIRT3‐medicated autophagy via the AMPK/mTOR/ULK1 pathway

Impaired Plakophilin-2 in obesity breaks cell cycle dynamics to breed adipocyte senescence

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