Changes in Steady-State Levels of Mrnas Coding for Type IV Collagen, Laminin and Fibronectin Following Capillary Basement Membrane Thickening in Human Adult Onset Diabetes

Kolbe, M; Kaufman, Jeffrey L.; Friedman, Julie; Dinerstein, Charles R.; Mackenzie, James W.; Boyd, Charles D.

doi:10.3109/03008209009009814

Cited by 19 publications

(9 citation statements)

References 21 publications

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“…The decreases in the levels of basement membrane components in the regenerating epidermis, which were consistent with those reported in several other studies [ 6 , 15 , 17 ], can be explained by the decreased mRNA expression of the genes encoding these components [ 30 ] and increased expression/activation of MMPs [ 31 – 33 ]. Immunohistochemistry for LM5 revealed structural abnormalities of the basement membrane including fragmentation and immaturity in hyperglycaemic rats.…”

Section: Discussionsupporting

confidence: 90%

Topical Administration of Acylated Homoserine Lactone Improves Epithelialization of Cutaneous Wounds in Hyperglycaemic Rats

Huang¹,

Minematsu²,

Kitamura³

et al. 2016

PLoS ONE

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Clinicians often experience delayed epithelialization in diabetic patients, for which a high glucose condition is one of the causes. However, the mechanisms underlying delayed wound closure have not been fully elucidated, and effective treatments to enhance epithelialization in patients with hyperglycaemia have not been established. Here we propose a new reagent, acylated homoserine lactone (AHL), to improve the delayed epithelialization due to the disordered formation of a basement membrane of epidermis in hyperglycaemic rats. Acute hyperglycaemia was induced by streptozotocin injection in this experiment. Full thickness wounds were created on the flanks of hyperglycaemic or control rats. Histochemical and immunohistochemical analyses were performed to identify hyperglycaemia-specific abnormalities in epidermal regeneration by comparison between groups. We then examined the effects of AHL on delayed epithelialization in hyperglycaemic rats. Histological analysis showed the significantly shorter epithelializing tissue (P < 0.05), abnormal structure of basement membrane (fragmentation and immaturity), and hypo- and hyperproliferation of basal keratinocytes in hyperglycaemic rats. Treating the wound with AHL resulted in the decreased abnormalities of basement membrane, normal distribution of proliferating epidermal keratinocytes, and significantly promoted epithelialization (P < 0.05) in hyperglycemic rats, suggesting the improving effects of AHL on abnormal epithelialization due to hyperglycemia.

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Section: Discussionsupporting

confidence: 90%

Topical Administration of Acylated Homoserine Lactone Improves Epithelialization of Cutaneous Wounds in Hyperglycaemic Rats

Huang¹,

Minematsu²,

Kitamura³

et al. 2016

PLoS ONE

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“…In this paradigm, NGF withdrawal correlates with increased JNK and p38 kinase activity (22). JNK and p38 kinase activity precede the induction of PC12 cell apoptosis, suggesting that kinase activation participates in the cell death pathway (22,23). Like PC12 cell apoptosis, JNK activation is important in the death of sympathetic neurons (24), T lymphocytes (25), and several cancer cell lines (26 -28).…”

mentioning

confidence: 99%

Bidirectional Regulation of p38 Kinase and c-Jun N-terminal Protein Kinase by Insulin-like Growth Factor-I

Cheng

Feldman

1998

Journal of Biological Chemistry

111

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We have previously shown that insulin-like growth factor I (IGF-I) activation of the IGF-I receptor rescues SH-SY5Y human neuroblastoma cells from high glucosemediated programmed cell death (PCD). In the current study, we further explored the potential points in the cell death cascade where IGF-I receptor activation may afford neuroprotection. As an initial step, we examined the effects of the PCD stimulus, high glucose, on stressactivated protein kinases, specifically the two mitogenactivated protein kinases p38 kinase and c-Jun N-terminal kinase (JNK). High glucose treatment activated the tyrosine phosphorylation of both p38 kinase and JNK in a dose-and time-dependent fashion. We next examined the effects of IGF-I on JNK and p38 kinase under normoglycemic and hyperglycemic conditions. IGF-I activated p38 kinase alone and had additive effects on glucose-induced p38 kinase phosphorylation. In contrast, IGF-I inhibited glucose activation of JNK phosphorylation and JNK activity. IGF-I also inhibited the glucoseinduced nuclear translocation of JNK, but did not effect glucose-induced translocation of p38 kinase. Finally, IGF-I inhibition of JNK phosphorylation was blocked by the mitogen-activated protein kinase/extracellular signal-regulated kinase inhibitor, PD98059. Collectively, these data imply cross-talk between the mitogen-activated protein kinase pathway and JNK and suggest that IGF-I activation of mitogen-activated protein kinases interferes with JNK activation and protects cells from PCD.The mitogen-activated protein (MAP) 1 kinases are a family of serine-threonine protein kinases that are activated in response to a variety of extracellular stimuli (1). The first members identified in the family were p42 and p44 extracellular signal-regulated kinases (ERKs), now known as ERK1 and ERK2, respectively. In the Ras pathway, phosphorylation of c-Raf 1 activates the downstream protein kinase, MAP kinase kinase 1 (also known as MAPK/ERK (MEK) or MKK1) or MAP kinase kinase 2 (MKK2). MKK1 and 2 activate ERK1 and ERK2, which leads to activation and translocation of ERKs to the nucleus. In the nucleus, the ERKs phosphorylate transcription factors, including Elk-1 and ATF-2. This signaling cascade is activated by growth factors and is important for cellular growth and mitogenesis (2).Another class of MAP kinase family members, the stressactivated c-Jun N-terminal kinases (JNKs), are primarily responsive to stressful stimuli. There are 10 identified isoforms of JNK originating from three homologous genes (JNK1, JNK2, and JNK3) with molecular masses of 46 or 54 kDa due to alternative splicing (3, 4). The Thr and Tyr sites of active phosphorylation are conserved between ERK and JNK; however, these sites are located within distinct phosphorylation motifs: Thr-Pro-Tyr (JNKs) and Thr-Glu-Try (ERKs) (5-7). JNK activation induces the phosphorylation of transcription factors, including c-Jun, Elk-1, and ATF-2, which regulate immediate early gene expression (4,8). Ultraviolet radiation, cytokines, and environmental stressors all ...

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“…The microvascular network of the skin is particularly altered in DM, and this worsens with age 15. The perivascular basement membranes are thickened, and the endothelial cells pile up 16,17. Type IV collagen and laminin are deposited in excess.…”

Section: Direct Skin Complications Of Dmmentioning

confidence: 99%

The skin landscape in diabetes mellitus. Focus on dermocosmetic management

Pierard¹,

Seité²,

Hermanns‐Lê³

et al. 2013

CCID

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BackgroundSome relationships are established between diabetes mellitus (DM) and a series of cutaneous disorders. Specific dermatoses are markers for undiagnosed DM. Other disorders represent supervening complications in an already treated DM patient.ObjectiveTo review the information about dermocosmetic care products and their appropriate use in the management and prevention of dermatoses related to DM.MethodThe peer-reviewed literature and empiric findings are covered. Owing to the limited clinical evidence available for the use of dermocosmetics, a review of the routine practices and common therapies in DM-related dermatoses was conducted.ResultsSome DM-related dermatoses (acanthosis nigricans, pigmented purpuric dermatosis) are markers of macrovascular complications. The same disorders and some others (xerosis, Dupuytren’s disease) have been found to be more frequently associated with microangiopathy. Other skin diseases (alopecia areata, vitiligo) were found to be markers of autoimmunity, particularly in type 1 DM. Unsurprisingly, using dermocosmetics and appropriate skin care has shown objective improvements of some DM-related dermatoses, such effects improve the quality of life. The most common skin manifestations of DM fall along continuum between “dry skin,” xerosis, and acquired ichthyosis, occurring predominately on the shins and feet. Dermocosmetic products improve the feeling of well-being for DM patients.

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Changes in Steady-State Levels of Mrnas Coding for Type IV Collagen, Laminin and Fibronectin Following Capillary Basement Membrane Thickening in Human Adult Onset Diabetes

Cited by 19 publications

References 21 publications

Topical Administration of Acylated Homoserine Lactone Improves Epithelialization of Cutaneous Wounds in Hyperglycaemic Rats

Topical Administration of Acylated Homoserine Lactone Improves Epithelialization of Cutaneous Wounds in Hyperglycaemic Rats

Bidirectional Regulation of p38 Kinase and c-Jun N-terminal Protein Kinase by Insulin-like Growth Factor-I

The skin landscape in diabetes mellitus. Focus on dermocosmetic management

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