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Articles by Mengmeng Liang
Total Records ( 2 ) for Mengmeng Liang
  Fengru Xi , Xiaoting Liu , Qian Wang and Mengmeng Liang
  Cost stickiness is an important economic phenomenon and an important factor that affects the business performance. Based on the classical Change Model of Anderson et al. (2003), this study analyzes and examines the impact of equity nature and the opportunism incentives from the management on the cost stickiness of listed companies in China. One of the features of this study is that it analyzes the influence of opportunism incentives on cost stickiness from the perspective of equity nature. According to the research results, the phenomenon of cost stickiness exists in most of the listed companies and the existence of opportunism incentives intensifies the cost stickiness behavior. Meanwhile, compared with the non-state-owned listed companies, the cost stickiness behaviors that happened in the state-owned companies are more serious, and thus are more likely to be influenced by the opportunism incentives.
  Chieh-Fang Cheng , Jianhua Fan , Mark Fedesco , Shengxi Guan , Yong Li , Balaji Bandyopadhyay , Alexandra M. Bright , Dalia Yerushalmi , Mengmeng Liang , Mei Chen , Yuan-Ping Han , David T. Woodley and Wei Li
  Jump-starting and subsequently maintaining epidermal and dermal cell migration are essential processes for skin wound healing. These events are often disrupted in nonhealing wounds, causing patient morbidity and even fatality. Currently available treatments are unsatisfactory. To identify novel wound-healing targets, we investigated secreted molecules from transforming growth factor α (TGFα)-stimulated human keratinoytes, which contained strong motogenic, but not mitogenic, activity. Protein purification allowed us to identify the heat shock protein 90α (hsp90α) as the factor fully responsible for the motogenic activity in keratinocyte secretion. TGFα causes rapid membrane translocation and subsequent secretion of hsp90α via the unconventional exosome pathway in the cells. Secreted hsp90α promotes both epidermal and dermal cell migration through the surface receptor LRP-1 (LDL receptor-related protein 1)/CD91. The promotility activity resides in the middle domain plus the charged sequence of hsp90α but is independent of the ATPase activity. Neutralizing the extracellular function of hsp90α blocks TGFα-induced keratinicyte migration. Most intriguingly, unlike the effects of canonical growth factors, the hsp90α signaling overrides the inhibition of TGFβ, an abundant inhibitor of dermal cell migration in skin wounds. This finding provides a long-sought answer to the question of how dermal cells migrate into the wound environment to build new connective tissues and blood vessels. Thus, secreted hsp90α is potentially a new agent for wound healing.
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