scispace - formally typeset
Search or ask a question
Author

Zhi Zhang

Bio: Zhi Zhang is an academic researcher from Jinan University. The author has contributed to research in topics: Hypertrophic scar & Decorin. The author has an hindex of 8, co-authored 25 publications receiving 319 citations.

Papers
More filters
Journal ArticleDOI
Zhi Zhang1, Xiaojian Li1, Yan Liu2, Xiong Zhang2, Ye-Yang Li1, Wei-Shi Xu2 
01 Aug 2007-Burns
TL;DR: Decorin has a down-regulatory effect on cell proliferation, TGF-beta(1) production, and collagen synthesis in hypertrophic scar fibroblasts, and improved understanding of such a regulatory mechanisms may eventually be of therapeutic significance in the control of hypertrophic Scarring.

109 citations

Journal ArticleDOI
01 Jun 2009-Burns
TL;DR: Decorin may have therapeutic potential for excessive skin contraction as observed in hypertrophic scarring, by using fibroblast-populated collagen lattice with decorin added to the collagen gel.

78 citations

Journal ArticleDOI
01 Mar 2012-Burns
TL;DR: The present study found that hypertrophic scar fibroblasts exhibited increased Smurf2 protein and mRNA levels compared with normal fibro Blasts, and the expression of SmurF2 gradually increased in hypertrophic Scar fibroBLasts after TGF-β1 stimulation, suggesting that the enhanced expression ofSmurf 2 is involved in the progression of hypertrophicScarring.

26 citations

Journal Article
Yan Liu1, Xiong Zhang, Zhi Zhang, Pei-Yao Fang, Wei-shi Xu 
TL;DR: Local injection of small dose of insulin may accelerate burn wound healing due to its role in promoting the proliferation and division of the repairing cells.
Abstract: OBJECTIVE: To investigate the effects of topical application of small dose of insulin on the wound healing of the scalded rats, so as to explore its mechanism. METHODS: The rats employed in the study were subjected to deep partial thickness burn and were divided into group A (with subcutaneous injection of isotonic saline into the rat wounds as control), B and C (with subcutaneous injection of 0.1 U and 1 U insulin in the rat wounds respectively) and D (with subcutaneous injection of 0.1 U insulin in the rat abdomen as control). The wound healing time and wound healing rate were assessed every other day after 3 postburn days (PBDs). The histological changes of the wounds after injection were examined, the changes in the cell cycle of epidermal cells in the wound were analyzed by flow-cytometry, and blood glucose concentration of each group was determined. RESULTS: The wound healing time in group B (18.36 +/- 4.12 d) was significantly shorter than that in other groups (A: 24.57 +/- 5.19 d, C: 21.46 +/- 2.97 d, D: 24.50 +/- 1.05 d, P < 0.01). The wound healing rate of the rats in group B in 5, 9, 11, 13, 15, 17 and 19 PBD was obviously higher than that in group A, and was markedly higher than that in group C on 17 PBD (P < 0.05 - 0.01). The epithelial layer was thinner with less epidermal nails but much more fibroblasts in epidermal layer in group A, while the epithelial layer was thicker with abundant epidermal nails in group B and C with many fibroblasts in the dermis. The amount of cells in S phase at 4 PBD in group B was dramatically higher than that in group A, and cells in G2M phase at 4 - 5 PBD in group B was also higher than that in group A and C (P < 0.05 - 0.01). The blood level of glucose in group A and B fluctuated between 3.42 to 4.62 mmol/L at 24 PBH, while that in group C and D decreased obviously 1 hour after injection (P < 0.01), but gradually returned to normal 4 hours after injection. CONCLUSION: Local injection of small dose of insulin may accelerate burn wound healing due to its role in promoting the proliferation and division of the repairing cells.

26 citations

Journal ArticleDOI
07 Feb 2014-PLOS ONE
TL;DR: The transplantation of ESCs- collagen- chitn biomimetic membrane (ESCs-C-CBM) has achieved in situ skin regeneration and indicates that the collagen-modified chitin membrane carry with ESCs has successfully regenerated the whole skin with all the skin appendages and function.
Abstract: A Large scale of full-thickness skin defects is lack of auto-grafts and which requires the engineered skin substitutes for repair and regeneration. One major obstacle in skin tissue engineering is to expand epidermal stem cells (ESCs) and develop functional substitutes. The other one is the scaffold of the ESCs. Here, we applied type I collagen-modified chitin membrane to form collagen-chitin biomimetic membrane (C-CBM), which has been proved to have a great biocompatibility and degraded totally when it was subcutaneously transplanted into rat skin. ESCs were cultured, and the resulting biofilm was used to cover full-thickness skin defects in nude mice. The transplantation of ESCs- collagen- chitn biomimetic membrane (ESCs-C-CBM) has achieved in situ skin regeneration. In nude mice, compared to controls with collagen-chitin biomimetic membrane (C-CBM) only, the ESCs-C-CBM group had significantly more dermatoglyphs on the skin wound 10 w after surgery, and the new skin was relatively thick, red and elastic. In vivo experiments showed obvious hair follicle cell proliferation in the full-thickness skin defect. Stem cell markers examination showed active ESCs in repair and regeneration of skin. The results indicate that the collagen-modified chitin membrane carry with ESCs has successfully regenerated the whole skin with all the skin appendages and function.

23 citations


Cited by
More filters
01 Jan 2016
TL;DR: Fibroblasts of high population doubling level propagated in vitro, which have left the cell cycle, can carry out the contraction at least as efficiently as cycling cells as discussed by the authors, and the potential uses of the system as an immu- nologically tolerated "tissue" for wound hea ing and as a model for studying fibroblast function are discussed.
Abstract: Fibroblasts can condense a hydrated collagen lattice to a tissue-like structure 1/28th the area of the starting gel in 24 hr. The rate of the process can be regulated by varying the protein content of the lattice, the cell number, or the con- centration of an inhibitor such as Colcemid. Fibroblasts of high population doubling level propagated in vitro, which have left the cell cycle, can carry out the contraction at least as efficiently as cycling cells. The potential uses of the system as an immu- nologically tolerated "tissue" for wound hea ing and as a model for studying fibroblast function are discussed.

1,837 citations

Journal ArticleDOI
TL;DR: The current understanding of the pathophysiology underlying keloid and hypertrophic scar formation is summarized and established treatments and novel therapeutic strategies are discussed.
Abstract: Excessive scars form as a result of aberrations of physiologic wound healing and may arise following any Insult to the deep dermis. By causing pain, pruritus and contractures, excessive scarring significantly affects the patient’s quality of life, both physically and psychologically. Multiple studies on hypertrophic scar and keloid formation have been conducted for decades and have led to a plethora of therapeutic strategies to prevent or attenuate excessive scar formation. However, most therapeutic approaches remain clinically unsatisfactory, most likely owing to poor understanding of the complex mechanisms underlying the processes of scarring and wound contraction. In this review we summarize the current understanding of the pathophysiology underlying keloid and hypertrophic scar formation and discuss established treatments and novel therapeutic strategies.

1,075 citations

Journal ArticleDOI
TL;DR: This review will focus on the components of the ECM and their role in both physiological and pathological (hypertrophic and keloid) cutaneous scar formation.
Abstract: Significance: When a cutaneous injury occurs, the wound heals via a dynamic series of physiological events, including coagulation, granulation tissue formation, re-epithelialization, and extracellular matrix (ECM) remodeling. The final stage can take many months, yet the new ECM forms a scar that never achieves the flexibility or strength of the original tissue. In certain circumstances, the normal scar is replaced by pathological fibrotic tissue, which results in hypertrophic or keloid scars. These scars cause significant morbidity through physical dysfunction and psychological stress. Recent Advances and Critical Issues: The cutaneous ECM comprises a complex assortment of proteins that was traditionally thought to simply provide structural integrity and scaffolding characteristics. However, recent findings show that the ECM has multiple functions, including, storage and delivery of growth factors and cytokines, tissue repair and various physiological functions. Abnormal ECM reconstruction during wound healing contributes to the formation of hypertrophic and keloid scars. Whereas adult wounds heal with scarring, the developing foetus has the ability to heal wounds in a scarless fashion by regenerating skin and restoring the normal ECM architecture, strength, and function. Recent studies show that the lack of inflammation in fetal wounds contributes to this perfect healing. Future Directions: Better understanding of the exact roles of ECM components in scarring will allow us to produce therapeutic agents to prevent hypertrophic and keloid scars. This review will focus on the components of the ECM and their role in both physiological and pathological (hypertrophic and keloid) cutaneous scar formation.

879 citations

05 Feb 2012
TL;DR: The role of growth factor TGF-β in the process of wound healing and scar formation has been investigated in this paper, showing that TGFβ1 was responsible for the fibrotic scarring response whereas the scarless wound healing seen in fetal wounds was due to increased levels of TGF β3.
Abstract: It is estimated worldwide that over 6 million people per annum experience a burn injury. Despite advances in management and improved survival rates, the incidence of hypertrophic scarring remains high. These scars are particularly common after burns and are often raised, red, hard and may cause abnormal sensations. Such pathological scarring can lead to severe functional impairment, psychological morbidity, and costly long term healthcare. Wound healing is an inherent process which restores the integrity of the skin after injury and although scarring is a frequent by-product, the scarless wound healing observed in early human gestational fetuses suggests that it is not an essential component of the response. This has lead to a large body of research attempting to understand the mechanisms behind scarring and in turn prevent it. One of the main focuses of recent research has been the role played by the growth factor TGF-β in the process of both wound healing and scar formation. The three isoforms (TGF-β1, TGF-β2 and TGF-β3) appear to have overlapping functions and predominantly mediate their effects through the intracellular SMAD pathway. Initial research suggested that TGF-β1 was responsible for the fibrotic scarring response whereas the scarless wound healing seen in fetal wounds was due to increased levels of TGF-β3. However, the reality appears to be far more complex and it is unlikely that simply altering the ratio of TGF-β isoforms will lead to scarless wound healing. Other aspects of the TGF-β system that appear promising include the downstream mediator CTGF, the proteoglycan decorin and the binding protein p311. Other putative mechanisms which may underlie the pathogenesis of hypertrophic scars include excessive inflammation, excessive angiogenesis, altered levels of matrix metalloproteinases, growth factors, and delayed apoptosis of fibrotic myofibroblasts either due to p53 genetic alterations or tensile forces across the wound. If an effective treatment for hypertrophic scars following burns injury is to be developed then further work must be carried out to understand the basic mechanisms of pathological scarring.

437 citations

Journal ArticleDOI
TL;DR: TGF‐β3 may offer a scar‐reducing therapy for acute and chronic wounds and fibrosing disorders.
Abstract: Scar formation, with persistent alteration of the normal tissue structure, is an undesirable and significant result of both wound healing and fibrosing disorders. There are few strategies to prevent or to treat scarring. The transforming growth factor beta (TGF-β) superfamily is an important mediator of tissue repair. Each TGF-β isoform may exert a different effect on wound healing, which may be context-dependent. In particular, TGF-β1 may mediate fibrosis in adults' wounds, while TGF-β3 may promote scarless healing in the fetus and reduced scarring in adults. Thus, TGF-β3 may offer a scar-reducing therapy for acute and chronic wounds and fibrosing disorders.

364 citations