Biology subjects

Ahn, H.-S.

Publications and source records attributed to Ahn, H.-S..

3 recordsLinked to original sources

bioRxiv2022

Stress-relief function of migrasomal autophagosomeformed by inhibition of autophagosome/lysosome fusion

Glioblastoma (GBM) is more difficult to treat than other intractable adult tumors. Here, we describe the composition and function of migrasomes generated along with GBM cell migration. Proteomic analysis revealed that LC3B-positive autophagosomes were abundant in the migrasomes of GBM cells. An increased number of migrasomes was observed following treatment with chloroquine (CQ) or inhibition of the expression of STX17 and SNAP29, which are involved in autophagosome/lysosome fusion. Although ATG7 ablation, which is involved in LC3B lipidation, did not suppress migrasome formation, it was confirmed that migrasome formation could be diminished by blocking the alternative autophagy pathway through double knockout of ATG7/BECN1. Furthermore, depletion of ITGA5 or TSPAN4 did not relieve endoplasmic reticulum (ER) stress in cells, resulting in cell death. Taken together, our study suggests that increasing the number of autophagosomes, through inhibition of autophagosome/lysosome fusion, generates migrasomes that have the capacity to alleviate cellular stress. Summary statementThis study demonstrates that glioblastoma cells contain autophagosomes within their migrasomes. Under stress conditions, the formation of migrasomes serves as a stress-relief mechanism to alleviate cell death.

cell biology↗

bioRxiv2020

CRP immunodeposition and proteomic analysis in abdominal aortic aneurysm

ObjectiveThe molecular mechanisms of the degeneration of the aortic wall in abdominal aortic aneurysm (AAA) are poorly understood. The monomeric form of C-reactive protein (mCRP) is deposited in damaged cardiovascular organs and aggravates the prognosis; however, it is unknown whether mCRP is deposited in the degenerated aorta of abdominal aortic aneurysm (AAA). We investigated whether mCRP is deposited in AAA and examined the associated pathogenic signaling pathways. MethodsTwenty-four cases of AAA were analyzed and their histological features were compared according to the level of serum CRP and the degree of mCRP deposition. Proteomic analysis was performed in AAA cases with strong and diffuse CRP immunopositivity (n=7) and those with weak, focal, and junctional CRP immunopositivity (n=3). ResultsmCRP was deposited in the aortic specimens of AAA in a characteristic pattern that coincided with the lesion of the diminished elastic layer of the aortic wall. High serum CRP level was associated with stronger mCRP immunopositivity and a larger maximal diameter of aortic aneurysm. Proteomic analysis in AAA showed that multiple proteins were differentially expressed according to mCRP immunopositivity. Also, ingenuity pathway analysis showed that pathways associated with atherosclerosis, acute phase response, complement system, immune system, and coagulation were enriched in AAA cases with high mCRP immunopositivity. ConclusionsAAA showed a characteristic deposition of mCRP, and multiple potentially pathologic signaling pathways were upregulated in AAA cases with strong CRP immunopositivity. mCRP and the aforementioned pathological pathways may serve as targets for managing the progression of AAA.

pathology↗

bioRxiv2019

Cell-type specificity of neuronal excitability and morphology in the central amygdala

Central amygdala (CeA) neurons expressing protein kinase C delta (PKC{delta}+) or Somatostatin (Som+) differentially modulate diverse behaviors. The underlying features supporting cell-type-specific function in the CeA, however, remain unknown. Using whole-cell patch-clamp electrophysiology in acute mouse brain slices and biocytin-based neuronal reconstructions, we demonstrate that neuronal morphology and relative excitability are two distinguishing features between Som+ and PKC{delta}+ CeLC neurons. Som+ neurons, for example, are more excitable, compact and with more complex dendritic arborizations than PKC{delta}+ neurons. Cell size, intrinsic membrane properties, and anatomical localization were further shown to correlate with cell-type-specific differences in excitability. Lastly, in the context of neuropathic pain, we show a shift in the excitability equilibrium between PKC{delta}+ and Som+ neurons, suggesting that imbalances in the relative output of these cells underlie maladaptive changes in behaviors. Together, our results identify fundamentally important distinguishing features of PKC{delta}+ and Som+ cells that support cell-type-specific function in the CeA.

neuroscience↗