Miroslav Blumenberg

Biosketch / Results /

Miroslav Blumenberg

Associate Professor, Ronald O. Perelman Department of Dermatology
Associate Professor, Department of Biochemistry and Molecular Pharmacology


Contact Info

Address
455 First Avenue
New York, NY 10016

212-263-5030
Miroslav.Blumenberg@nyumc.org

Research Summary


DNA microarrays allow us to follow global cellular responses to various agents. Using UV light as a paradigmatic damaging agent, we determined that cells make following responses: 1. They change signal transduction and transcription regulators, basically stop what they have been doing and respond to UV. 2. Produce cytokines and chemokine to alert the surrounding tissue to the damage. 3. Produce more energy by increasing mitochondrial proteins and suppressing proteins that use energy. 4. Increase the cornified layer that protects the skin. These responses protect not only the cells, but also the underlying tissues of the organism.

In another study, we described the antiviral effects of Interferon-gamma in skin. Specifically, we found that IFNg suppresses cell cycle and DNA replication ? the cell that does not replicate its own DNA will not replicate the viral either; IFNg boosts tight junction proteins, impeding para-cellular viral entry into the organism, and suppresses epidermal differentiation, which inhibits proliferation of papilloma viruses.
We are extending our studies to other agents that affect skin biology, such as proinflammatory cytokines, DNA damaging agents etc. Recently, we have started a program focused on epidermal stem cells and differentiation. Our goal is to describe the global molecular responses of skin to its environment.

Research Keywords

molecular biology and genetics of human keratin genes, transcriptional profiling of skin cells using DNA microarrays, effects of UV light on skin, signal transduction in skin during inflammatory and proliferative processes, epidermal stem cells and differentiation

A bioengineered living cell construct activates an acute wound healing response in venous leg ulcers
Stone, Rivka C; Stojadinovic, Olivera; Rosa, Ashley M; Ramirez, Horacio A; Badiavas, Evangelos; Blumenberg, Miroslav; Tomic-Canic, Marjana. A bioengineered living cell construct activates an acute wound healing response in venous leg ulcers. Science translational medicine. 2017 Jan 4;9(371):?-? (2386732)

Cyclic amp, ERK5, and transdifferentiation of cardiac fibroblasts in the pathogenesis of autoimmune congenital heart block
Markham, A; Rasmussen, S; Blumenberg, M; Clancy, R M; Buyon, J P. Cyclic amp, ERK5, and transdifferentiation of cardiac fibroblasts in the pathogenesis of autoimmune congenital heart block [Meeting Abstract]. Arthritis & rheumatology. 2016 October;Conference:(American):3179-3181 (2398042)

Transcriptome profile of cells isolated from a CHB heart support an exuberant inflammatory/pro-fibrotic cascade
Clancy, R M; Markham, A; Jackson, T A; Rasmussen, S; Blumenberg, M; Buyon, J P. Transcriptome profile of cells isolated from a CHB heart support an exuberant inflammatory/pro-fibrotic cascade [Meeting Abstract]. Arthritis & rheumatology. 2016 October;Conference:(American):3240-3242 (2398142)

The homeoprotein DLX3 and tumor suppressor p53 co-regulate cell cycle progression and squamous tumor growth
Palazzo, E; Kellett, M; Cataisson, C; Gormley, A; Bible, P W; Pietroni, V; Radoja, N; Hwang, J; Blumenberg, M; Yuspa, S H; Morasso, M I. The homeoprotein DLX3 and tumor suppressor p53 co-regulate cell cycle progression and squamous tumor growth. Oncogene. 2016 Jun 16;35(24):3114-3124 (2009752)

Keratinocyte p38delta loss inhibits Ras-induced tumor formation, while systemic p38delta loss enhances skin inflammation in the early phase of chemical carcinogenesis in mouse skin
Kiss, Alexi; Koppel, Aaron C; Anders, Joanna; Cataisson, Christophe; Yuspa, Stuart H; Blumenberg, Miroslav; Efimova, Tatiana. Keratinocyte p38delta loss inhibits Ras-induced tumor formation, while systemic p38delta loss enhances skin inflammation in the early phase of chemical carcinogenesis in mouse skin. Molecular carcinogenesis. 2016 May;55(5):563-574 (1494682)