↓ Skip to main content

RIP1K Contributes to Neuronal and Astrocytic Cell Death in Ischemic Stroke via Activating Autophagic-lysosomal Pathway

Overview of attention for article published in Neuroscience, February 2018
Altmetric Badge

Mentioned by

twitter
1 tweeter

Citations

dimensions_citation
20 Dimensions

Readers on

mendeley
28 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
RIP1K Contributes to Neuronal and Astrocytic Cell Death in Ischemic Stroke via Activating Autophagic-lysosomal Pathway
Published in
Neuroscience, February 2018
DOI 10.1016/j.neuroscience.2017.10.038
Pubmed ID
Authors

Yong Ni, Wei-Wei Gu, Zhi-He Liu, Yong-Ming Zhu, Jia-Guo Rong, Thomas A. Kent, Min Li, Shi-Gang Qiao, Jian-Zhong An, Hui-Ling Zhang

Abstract

Although the receptor-interacting protein 1 kinase (RIP1K)-regulated necroptosis can be evoked by cerebral ischemia, the effects of RIP1K in mediating neuronal and astrocytic cell death and the underlying mechanisms remain poorly understood. This study evaluates the contribution of RIP1K to ischemic stroke-induced neuronal and astrocytic cell death, and the activation of autophagic-lysosomal pathway. Using an in vitro oxygen and glucose deprivation (OGD) in primary cultured neurons or astrocytes and a permanent middle cerebral artery occlusion (pMCAO) model in rats or mice, we observed the role of RIP1K in the ischemic neuronal and astrocytic cell death and the underlying mechanisms by pharmacological or genetic inhibition of RIP1K. pMCAO or OGD condition led to an increase in RIP1K, RIP3K and RIP1K-RIP3K complex. RIP1K knockdown or necrostatin-1 (Nec-1, a specific inhibitor of RIP1K) treatment reduced infarct volume, improved neurological deficits, increased microtubule-associated protein 2 (MAP2) and glial fibrillary acidic protein (GFAP) levels, and attenuated neuronal or astrocytic necrotic cell death in the ischemic cortex. RIP1K knockdown decreased RIP1K-RIP3K complex formation, light chain 3 II (LC3II) and active cathepsin B levels and lysosomal membrane permeability (LMP). Furthermore, a combination of Nec-1 and an inhibitor of autophagy or cathepsin B produced an enhancement of protective effect on neuronal or astrocytic cell death. RIP1K-mediated necroptosis may play important roles in ischemia-induced neuronal and astrocytic cell death through the activation of autophagic-lysosomal pathway.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 28 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 28 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 7 25%
Student > Bachelor 5 18%
Student > Ph. D. Student 4 14%
Student > Master 4 14%
Student > Doctoral Student 1 4%
Other 2 7%
Unknown 5 18%
Readers by discipline Count As %
Neuroscience 8 29%
Medicine and Dentistry 6 21%
Agricultural and Biological Sciences 4 14%
Biochemistry, Genetics and Molecular Biology 3 11%
Immunology and Microbiology 1 4%
Other 1 4%
Unknown 5 18%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 06 November 2017.
All research outputs
#13,290,422
of 15,046,426 outputs
Outputs from Neuroscience
#5,554
of 6,306 outputs
Outputs of similar age
#272,006
of 320,502 outputs
Outputs of similar age from Neuroscience
#97
of 113 outputs
Altmetric has tracked 15,046,426 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 6,306 research outputs from this source. They receive a mean Attention Score of 4.6. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 320,502 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 113 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.