Two distinct phases of calcium signalling under flow

Liu, Bo; Lu, Shaoying; Zheng, Shuai; Jiang, Zong‐Lai; Wang, Yingxiao

doi:10.1093/cvr/cvr033

Cited by 46 publications

(35 citation statements)

References 52 publications

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“…Previous reports showed that glycerophosphatidylcholine concentration typically increases with age; moreover, this increase is more pronounced in aged AD patients and those with enhanced A ␤ plaque formation (29)(30)(31)(32). Breakdown of APP and aggregation of amyloid plaques are the major causes of neuronal deterioration in AD.…”

Section: Discussionmentioning

confidence: 98%

Global changes of phospholipids identified by MALDI imaging mass spectrometry in a mouse model of Alzheimer's disease

Hong

Kang

Kim

et al. 2016

Journal of Lipid Research

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This article is available online at http://www.jlr.org Several hypotheses regarding the cause of AD have been proposed, among which the amyloid hypothesis is the most widely accepted ( 2 ). According to this hypothesis, AD is caused by abnormal accumulation of misfolded ␤ -amyloid (A ␤ ), a sequential cleavage product produced from amyloid precursor protein (APP) by ␤ -and ␥ -secretases, and hyperphosphorylated tau protein. Several lines of evidence support the idea that A ␤ can trigger the hyperphosphorylation of tau, resulting in neuronal degeneration in the brain ( 3, 4 ).There is evidence that FFAs are associated with several signaling processes related to the pathogenesis of AD. In particular, palmitic and stearic acid induce AD by triggering hyperphosphorylation of tau protein ( 5 ). Membrane phospholipids (PLs) are a prominent source of FFAs. Under disease conditions, phospholipase enzymes are produced in excess, inducing the hydrolysis of PLs and the release of FFAs. It is reasonable to hypothesize that alterations in PL concentrations are closely related to the pathogenesis of AD, as PLs perform a number of important cellular roles, including stabilization of membrane ion channels, neurotransmission, and the localization of A ␤ plaques to PL cores ( 6, 7 ).As a result of progress in MS, and MALDI-imaging MS (IMS) in particular, the analysis of PL changes during disease progression has become feasible. MALDI-IMS is a unique tool that integrates molecular and histological information together with information attained using Alzheimer's disease (AD), the most common form of dementia, is primarily caused by abnormal protein kinesis and the accumulation of aggregated proteins in the brain. This work was supported

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Section: Discussionmentioning

confidence: 98%

Global changes of phospholipids identified by MALDI imaging mass spectrometry in a mouse model of Alzheimer's disease

Hong

Kang

Kim

et al. 2016

Journal of Lipid Research

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“…The signaling pathway of PLC activatedcalcium release from ER has been discovered in wide cell lineages such as endothelial cells, 24 osteoblasts 32 as well as osteoclasts. 38 For this signaling pathway, PLC first activates IP3 and then IP3 binds with IP3R in ER membrane finally leading to the efflux of calcium from ER stores.…”

Section: Discussionmentioning

confidence: 99%

Fluid Flow-Induced Calcium Response in Osteoclasts: Signaling Pathways

Liu

et al. 2014

Ann Biomed Eng

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Abstract-Intracellular calcium oscillation and its downstream signaling in osteoclasts is believed to play critical roles in regulating bone resorption. Our previous study demonstrated that fluid shear stress (FSS) induced more calcium responsive peaks in the late differentiated osteoclasts than the early ones. In this paper, the signaling pathways of FSS-induced calcium response for the osteoclasts in different differentiation stages were studied. RAW264.7 macrophage cells were induced to differentiate into osteoclasts with the conditioned medium from MC3T3-E1 osteoblasts. Furthermore pharmacological agents were added to block the specific signaling pathways. Finally the cells were exposed to FSS at different levels (1 or 10 dyne/cm 2 ) after being induced for 4 or 8 days. The results showed that the mechanosensitive, cation-selective channels, phospholipase C (PLC) and endoplasmic reticulum constituted the major signaling pathway for mechanical stimulation-induced calcium response in osteoclasts. Extracellular calcium or ATP involved with calcium oscillation in a FSS magnitude-dependent manner. This pathway study may help to give insight into the molecular mechanism of mechanical stimulation-regulated bone remodeling.

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“…Every contraction stroke is associated with a pulsatile fluid movement, a nonlaminar lymph flow due to the presence of valves. The subsequent shear stress stimulates endothelial cells, which modulate LSMCs contraction [63,64]. However, there are several limitations to interpreting the role of shear stress in this process.…”

Section: Propelling the Lymph Down The Road: The Physiology Of The Comentioning

confidence: 99%

Lymphatic Network in Atherosclerosis: the Underestimated Path

2015

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The lymphatic system is a key component of tissue fluid homeostasis. In contrast to the closed and high-pressure blood vascular system, the lymphatic vascular system transports lymph in an open and low-pressure network. A prerequisite player in the transport of immune cells and cholesterol metabolism, it has been understudied until recently. Whereas defects in lymph circulation are mostly associated with pathologies such as congenital or acquired lymphedema, emerging significant developments are unraveling the role of lymphatic vessels in other pathological settings. In the last decade, discoveries of underlying genes responsible for developmental and postnatal lymphatic growth, combined with state-of-the-art lymphatic function imaging and quantification techniques, have matched the growing interest in understanding the role of the lymphatic system in atherosclerosis. With a historical perspective, this review highlights the current knowledge regarding interaction between the lymphatic vascular tree and atherosclerosis, with an emphasis on the physiological mechanisms of this multifaceted system throughout disease onset and progression.

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Two distinct phases of calcium signalling under flow

Cited by 46 publications

References 52 publications

Global changes of phospholipids identified by MALDI imaging mass spectrometry in a mouse model of Alzheimer's disease

Global changes of phospholipids identified by MALDI imaging mass spectrometry in a mouse model of Alzheimer's disease

Fluid Flow-Induced Calcium Response in Osteoclasts: Signaling Pathways

Lymphatic Network in Atherosclerosis: the Underestimated Path

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