Organellar Dynamics in Cell Fate

Editorial

05 August 2022

Editorial: Organellar dynamics in cell fate

Yuzhen Li

Xianglan Yao

Stewart J. Levine

and

Sang-Bing Ong

1,685 views

0 citations

Editors

Yuzhen Li

People's Liberation Army General Hospital

Xianglan Yao

Clinical Center (NIH)

Stewart J. Levine

National Heart, Lung, and Blood Institute (NIH)

Sang-Bing Ong

Department of Medicine and Therapeutics, Faculty of Medicine, The Chinese University of Hong Kong

Impact

Temporal control of the WNT signaling pathway determined the efficiency and yield of cardiac differentiation. Human PSCs were differentiated using different differentiation protocols. (A) Representative flow cytometric analysis of MD1-C16 derived CMs and (B) graphs showed the proportion of TNNT2+ cells on day 15 of differentiation. Blue and red histograms represent isotype and TNNT2+ staining respectively (n = 5). (C) Live cell yield of hPSC-CM cultures presented as the average of independent experiments (n = 3–4). (D) Representative flow cytometric analysis of MD1-C16 derived CMs and (E) graphs showed the proportion of TNNT2+ cells on day 30 of differentiation. (n = 3).

Original Research

24 March 2022

Temporal Control of the WNT Signaling Pathway During Cardiac Differentiation Impacts Upon the Maturation State of Human Pluripotent Stem Cell Derived Cardiomyocytes

Chantelle Tsoi

, 10 more and

Ellen N. Poon

5,340 views

9 citations

Downregulation of Lnc-FR332443 and Runx1 expression during adipogenic differentiation. (A) Oil red O staining of mouse 3T3-L1 preadipocyte adipogenic differentiation at days 0, 2, 4, 6, and 8. Scale bar, 200 μm. (B) The Lnc-FR332443 and Runx1 mRNA levels during 3T3-L1 preadipocyte differentiation on different days. (C) Western blot analysis of Runx1 and adipogenic marker (anti-PPARγ and anti-C/EBPα) protein levels in 3T3-L1 preadipocytes differentiated on different days. (D) The quantification data of panel (C). (E) The time course of Lnc-FR332443 and Runx1 mRNA expression during 3T3-L1 preadipocyte differentiation after infection with lentivirus-Lnc-FR332443. (F) Western blots of Runx1 protein expression in the 3T3-L1 preadipocytes differentiated on different days after lentivirus-Lnc-FR332443 infection. (G) The quantification data of panel (F). All the data are shown as the mean ± SEM, NS denotes not significant, N = 3, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.

Original Research

08 June 2021

Long Non-coding RNA 332443 Inhibits Preadipocyte Differentiation by Targeting Runx1 and p38-MAPK and ERK1/2-MAPK Signaling Pathways

Fen Xiao

, 5 more and

Hou-De Zhou

3,684 views

13 citations

The activation of CaMKIIδB and CaMKIIδC in cardiomyocyte during pathological condition.

Review

01 June 2021

CaMKII in Regulation of Cell Death During Myocardial Reperfusion Injury

Yingjie Yang

, 3 more and

Yaozu Xiang

7,129 views

25 citations

Review

07 May 2021

Mitochondrial Fusion Protein Mfn2 and Its Role in Heart Failure

Lei Chen

, 5 more and

Guohua Gong

Mitofusin 2 (Mfn2) is a transmembrane GTPase located on the mitochondrial outer membrane that contributes to mitochondrial network regulation. It is an essential multifunctional protein that participates in various biological processes under physical and pathological conditions, including mitochondrial fusion, reticulum–mitochondria contacts, mitochondrial quality control, and apoptosis. Mfn2 dysfunctions have been found to contribute to cardiovascular diseases, such as ischemia-reperfusion injury, heart failure, and dilated cardiomyopathy. Here, this review mainly focuses on what is known about the structure and function of Mfn2 and its crucial role in heart failure.

8,916 views

48 citations

$Overexpression of caspase-1 abrogates the salutary effects of hypertrophic preconditioning in pressure overload hearts. (A) Gross appearance of the hearts. Scale bar, 1 mm. (B) Cardiomyocytes stained by HE. Scale bar, 20 μm. (C), Cardiomyocytes stained by WGA. Scale bar, 20 μm. (D) Interstitial fibrosis stained by Masson’s trichrome. Scale bar, 100 μm. (E) Perivascular fibrosis stained by Masson’s trichrome. Scale bar, 50 μm. (F), M-mode echocardiograms of left ventricles. (G) Left ventricular contraction and relaxation velocity images measured by a Millar catheter. Scale bar, 1s. (H) Peak systolic velocity of aortic arch flow (PSVa). (I) Heart rate. (J) Ratio of heart weight and body weight (HW/BW). (K) Left ventricular end-diastolic dimension (LVEDD). (L) Left ventricular end-systolic dimension (LVESD). (M) Left ventricular posterior wall end-diastolic thickness (LVPWTd). (N) Left ventricular posterior wall end-systolic thickness (LVPWTs). (O) CSAs of cardiomyocytes. (P) Quantitative interstitial fibrosis. (Q) Quantitative perivascular fibrosis. (R, S) Real-time quantitative PCR analyses for the expression of ANP and BNP, respectively. (T) Left ventricular ejection fraction (LVEF). (U) Left ventricular fractional shortening (LVFS). (V) Left ventricular end-systolic pressure (LVESP). (W) Left ventricular end-diastolic pressure (LVEDP). (X) Maximal +dp/dt (Y). Minimal -dp/dt. n = 4. *p < 0.05 vs. Sham+EGFP (Enhanced Green Fluorescent Protein, EGFP) or Sham+Casp1 (caspase-1 overexpression, Casp1), †p < 0.05 vs. Re-TAC+EGFP, two-way ANOVA.$