Profile

Chief Doctor of Pediatric Neurology

*Education/ Training:
MD, PhD, Zhejiang University (2004)
Visiting Associate Professor, Department of Neurosurgery School of Medicine, Stanford University (2006.12-2009.1)

*Research Interests:
Our lab is interested in I) organization and plasticity of cortical circuits, II) epileptogenesis following multiple injury in immature brain, and III) the mechanisms underlying the cerebral injury and functional recovery after stroke. These topics are investigated with a variety of techniques at molecular, cellular and circuit levels, including laser scanning photostimulation combined with whole cell patch clamp recording, organotypic brain slice culture, gene gun transfection, confocal imaging, and molecular biological techniques. The long-term goals of the lab are to understand the molecular and cellular mechanisms of epileptogenesis, and brain injury / repair after ischemia, for development of therapeutic strategies against epilepsy and stroke in children.

*Current Studies Include:

A) Glial ATP-sensitive potassium (K-ATP) channels regulate astroglial metabolic networks in response to neuronal activity in rat brain. One of the most basic parameters for neuronal activity is energy metabolism, thus the abnormalities of cerebral energy metabolism may result in brain dysfunction which known to be closely relate to neuronal diseases. The activities of hippocampal neurons were energy-dependent with the energy transported through the gap junction(GJ)-coupled astroglial metabolic networks. K-ATP channels couple cell metabolism to electrical activity, and we have confirmed that glial K-ATP channels can influence GJ couplings. We explore: I. The regulation of glial K-ATP channels on energy transportation coupled by the astroglial metabolic networks; II. Neuronal activity is astroglial metabolic network-dependent which mainly regulated by glial K-ATP channels, and its subsequently excitatory / inhibitory receptor-mediated pathways.

B) Understanding the mapping and regulation of cortical circuits following multiple injury in immature brain. As the concept of a network of injury has emerged in the treatment of epilepsy, the importance of evaluating that network noninvasively has also grown. Recently, studies utilizing functional (f)MRI measures of resting state connectivity have demonstrated their ability to detect injury and dysfunction in cerebral networks involved in the propagation of seizures. We use a combination of fMRI measures of resting state connectivity and glutamate uncaging with whole cell patch clamp recording techniques to study the organization of neural circuits in the neocortex, particularly the long-range corticocortical connections between somatosensory and motor cortices.

*Publications:
[1]　 Jiang KW, Wang JP, Zhao CY, Feng M, Shen Z, Yu ZS, Xia ZZ. Regulation of Gap Junctional Communication by Astrocytic Mitochondrial KATP Channels following Neurotoxin Adminstration in Vitro and in Vivo Models. NeuroSignals. 2011, 19(2): 63-74.[2] Horie N, Pereira MP, Niizuma K, Sun G, Keren-Gill H, Encarnacion A, Shamloo M, Hamilton SA, Jiang KW, Huhn S, Palmer TD, Bliss TM, Steinberg GK. Transplanted Stem Cell-Secreted VEGF Effects Post-Stroke Recovery, Inflammation, and Vascular Repair. Stem Cells. 2011, 29(2):274-285.
[3] Daadi MM, Davis AS, Arac A, Li Z., Maag AL, Bhatnagar R, Jiang KW, Sun G, Wu JC and Steinberg GK. Human Neural Stem Cell Grafts Modify Microglial Response and Enhance Axonal Sprouting in Neonatal Hypoxic-Ischemic Brain Injury. Stroke.2010, 41(3):516-23.
[4] Xu YP, Zhu JJ, Cheng F, Jiang KW, Gu WZ, Shen Z, Wu YD, Liang L, Du LZ. Ghrelin ameliorates hypoxia-induced pulmonary hypertension via phospho-GSK3 β/β-catenin signaling in neonatal rats.J Mol Endocrinol. 2011, 18;47(1):33-43.
[5] Dai YW, Lin L, Tang HF, Jiang KW. Follicular bronchiolitis in a child. World J Pediatr. 2011, 7(2):176-178.
[6] Gao F, Ma FC, Yuan ZF, Yang CW, Li HF, Xia ZZ, Shui QX, Jiang KW, Novel chloride channel gene mutations in two unrelated Chinese families with myotonia congenita. Neurol India, 2011, 58:743-746.
[7] Jiang KW, Yu ZS, and Shui QX. The pattern of ATP-sensitive K+ channel subunits, Kir6.2 and SUR1 mRNA expressions in DG region is different from those in CA1-3 regions of chronic epilepsy induced by picrotoxin in rats, Neuropathology 27 (2007) 531-538.
[8] Jiang KW, Shui QX, and Xia ZZ. Time-course of μ-calpain activation, c-Fos, c-Jun, HSP70 and HSP27 expression in neonatal hypoxic-ischemic rat brain. World Journal of Pediatrics. 2006（1）60-65.
[9] Jiang KW, Shui QX, Xia ZZ, and Yu ZS. Changes in the gene and protein expression of K(ATP) channel subunits in the hippocampus of rats subjected to picrotoxin-induced kindling, Brain Res Mol Brain Res 128 (2004) 83-89.
[10] Jiang KW, Zhao ZY, Shui QX, and Xia ZZ. Electro-acupuncture preconditioning abrogates the elevation of c-Fos and c-Jun expression in neonatal hypoxic-ischemic rat brains induced by glibenclamide, an ATP-sensitive potassium channel blocker, Brain Res 998 (2004) 13-19.
[11] Jiang KW, Gao F, Shui QX, Yu ZS, and Xia ZZ. Effect of diazoxide on regulation of vesicular and plasma membrane GABA transporter genes and proteins in hippocampus of rats subjected to picrotoxin-induced kindling, Neurosci Res 50 (2004) 319-329.
[12] Jiang KW, Yu ZS, Shui QX and Xia ZZ, Activation of ATP-sensitive potassium channels prevents the cleavage of cytosolic mu-calpain and abrogates the elevation of nuclear c-Fos and c-Jun expressions after hypoxic-ischemia in neonatal rat brain, Brain Res Mol Brain Res 133 (2005) 87-94.