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Upregulation of myeloid cell leukemia-1 potentially modulates beclin-1-dependent autophagy in ischemic stroke in rats.
BMC Neurosci 2013; 14:56BN

Abstract

BACKGROUND

The mechanisms that underlie autophagy in cerebral ischemia remain poorly defined. Myeloid cell leukemia-1 (Mcl1), an anti-apoptotic member of the Bcl-2 family of proteins, regulates the balance between autophagy and apoptosis. However, little is known regarding its expression profile and contribution to cell fate in the brain following ischemic stroke.

RESULTS

In this study, we investigated the expression profile and cellular distribution of Mcl1 in brains from transient middle cerebral artery occlusion (MCAO) model rats. Brain slices from sham-operated control rats showed minimal immunoreactivity for Mcl1. Mcl1 was mainly produced in neurons. Immunoreactivity for Mcl1 increased as early as 4 hours after MCAO, peaked at 24 hours, and then declined, but still remained high, at 72 hours. Mcl1 positive cells never colocalized with either cleaved caspase-3 or terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cells. Both microtubule-associated protein 1 light chain 3 (LC3) and beclin-1 were evident in ischemic brain between 4 and 72 hours after MCAO. Most cells with strong LC3 staining were also labeled with beclin-1. Beclin-1 did colocalize with caspase-3 or Mcl1. Beclin-1/caspase-3 positive cells displayed the characteristic features of apoptosis including cell shrinkage and pyknotic nuclei, whereas beclin-1/Mcl1 positive cells had normal morphology. Pretreatment with 3-methyladenine attenuated autophagy without affecting the level of Mcl1 protein.

CONCLUSIONS

These findings demonstrate that the expression of Mcl1 is involved in the survival of neuronal cells. In addition, the coexpression of Mcl1 with beclin-1 may attenuate beclin-1-dependent autophagy during ischemic stroke in rats.

Authors+Show Affiliations

Department of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23688351

Citation

Xingyong, Chen, et al. "Upregulation of Myeloid Cell Leukemia-1 Potentially Modulates Beclin-1-dependent Autophagy in Ischemic Stroke in Rats." BMC Neuroscience, vol. 14, 2013, p. 56.
Xingyong C, Xicui S, Huanxing S, et al. Upregulation of myeloid cell leukemia-1 potentially modulates beclin-1-dependent autophagy in ischemic stroke in rats. BMC Neurosci. 2013;14:56.
Xingyong, C., Xicui, S., Huanxing, S., Jingsong, O., Yi, H., Xu, Z., ... Zhong, P. (2013). Upregulation of myeloid cell leukemia-1 potentially modulates beclin-1-dependent autophagy in ischemic stroke in rats. BMC Neuroscience, 14, p. 56. doi:10.1186/1471-2202-14-56.
Xingyong C, et al. Upregulation of Myeloid Cell Leukemia-1 Potentially Modulates Beclin-1-dependent Autophagy in Ischemic Stroke in Rats. BMC Neurosci. 2013 May 20;14:56. PubMed PMID: 23688351.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Upregulation of myeloid cell leukemia-1 potentially modulates beclin-1-dependent autophagy in ischemic stroke in rats. AU - Xingyong,Chen, AU - Xicui,Sun, AU - Huanxing,Su, AU - Jingsong,Ou, AU - Yi,Huang, AU - Xu,Zhang, AU - Ruxun,Huang, AU - Zhong,Pei, Y1 - 2013/05/20/ PY - 2012/09/04/received PY - 2013/05/16/accepted PY - 2013/5/22/entrez PY - 2013/5/22/pubmed PY - 2013/11/2/medline SP - 56 EP - 56 JF - BMC neuroscience JO - BMC Neurosci VL - 14 N2 - BACKGROUND: The mechanisms that underlie autophagy in cerebral ischemia remain poorly defined. Myeloid cell leukemia-1 (Mcl1), an anti-apoptotic member of the Bcl-2 family of proteins, regulates the balance between autophagy and apoptosis. However, little is known regarding its expression profile and contribution to cell fate in the brain following ischemic stroke. RESULTS: In this study, we investigated the expression profile and cellular distribution of Mcl1 in brains from transient middle cerebral artery occlusion (MCAO) model rats. Brain slices from sham-operated control rats showed minimal immunoreactivity for Mcl1. Mcl1 was mainly produced in neurons. Immunoreactivity for Mcl1 increased as early as 4 hours after MCAO, peaked at 24 hours, and then declined, but still remained high, at 72 hours. Mcl1 positive cells never colocalized with either cleaved caspase-3 or terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cells. Both microtubule-associated protein 1 light chain 3 (LC3) and beclin-1 were evident in ischemic brain between 4 and 72 hours after MCAO. Most cells with strong LC3 staining were also labeled with beclin-1. Beclin-1 did colocalize with caspase-3 or Mcl1. Beclin-1/caspase-3 positive cells displayed the characteristic features of apoptosis including cell shrinkage and pyknotic nuclei, whereas beclin-1/Mcl1 positive cells had normal morphology. Pretreatment with 3-methyladenine attenuated autophagy without affecting the level of Mcl1 protein. CONCLUSIONS: These findings demonstrate that the expression of Mcl1 is involved in the survival of neuronal cells. In addition, the coexpression of Mcl1 with beclin-1 may attenuate beclin-1-dependent autophagy during ischemic stroke in rats. SN - 1471-2202 UR - https://www.unboundmedicine.com/medline/citation/23688351/Upregulation_of_myeloid_cell_leukemia_1_potentially_modulates_beclin_1_dependent_autophagy_in_ischemic_stroke_in_rats_ L2 - https://bmcneurosci.biomedcentral.com/articles/10.1186/1471-2202-14-56 DB - PRIME DP - Unbound Medicine ER -