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Raimund
Hirschberg, MD
Professor of Medicine
Department of
Medicine
Division of Nephrology & Hypertension
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| Office Address:
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Harbor-UCLA Medical
Center, Box 406
1000 West Carson St
Torrance, CA 90509
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| Office Phone: |
(310) 222-3891
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| Fax: |
(310) 782-1837
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| Lab Address: |
Harbor-UCLA REI,
C-1-Annex
1124 West Carson St
Torrance, CA 90502 |
| Lab Phone: |
(310) 222-3891
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| Email Address:
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rhirschberg@rei.edu
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Degree:
Undergraduate
Institutions:
- Rheinisch-Westphaelische Technische Hochschule
Aachen,
Germany
- Free University of
Berlin
(West) Berlin, Germany
Graduate
Institution:
- Free University of
Berlin - School of Medicine
(West) Berlin, Germany
Residency
Institution:
- St. Joseph
Hospital
Berlin, Germany
Post-Doctoral
Fellowship Institutions:
- St. Joseph
Hospital
Berlin, Germany
- Harbor-UCLA
Medical Center
Torrance, CA
Board
Certifications:
- Internal
Medicine
- Nephrology
Areas of Clinical
Interest:
- Clinical
Nephrology
- Hypertension
- Acute Renal
Replacement Therapies
Areas of Research
Interest:
- Tubular Epithelial
Cell Activation and Transdifferentiation
- Cytokines/Growth
Factors in the kidney (IGF-I, TGF-beta, BMPs)
- Renal Interstitial
Fibrosis
- Diabetic
Nephropathy
- Acute Renal
Failure
Specialized
Techniques in Research:
- General Cell and
Molecular Techniques
- in-vitro Cell
Transfection
- rtPCR
- Northern and
Western Blot Analysis
- Immunohisto- and
Cytochemistry
Research
Focus:
Renal tubular epithelial cells are exposed to both apical as
well as basolateral, normal or abnormal biological signals. For example,
in glomerular proteinuria ultrafiltered, bioactive proteins (IGF-I,
TGF-beta, HGF) can ‘activate’ tubular cells through interaction with
specific receptors in the apical membrane causing basolateral events
(secretion of C-C-chemokines such as MCP-1 and Rantes, cytokines such as
PDGF-B and others) that act on interstitial myofibroblasts and attracted
macrophages. The interaction between these three cell types can
contribute to accumulation of ECM-proteins and, hence, progressive renal
interstitial fibrosis.
Under certain conditions such as in experimental diabetic
nephropathy, tubular cells may change their overall gene expression
program and transdifferentiate towards a mesenchymal phenotype. Members
of the cystine-knot superfamily of secreted cytokine genes (TGF-beta,
BMPs) and their receptors seem to play key roles in these processes and
are a focus of our research. The mechanisms participating in induction
and maintenance of these phenotypic changes and their contributions to
renal interstitial fibrosis are also studied in the laboratory. We use
cell biologic and molecular approaches and experimental in-vitro and
in-vivo models to better understand the interplay of tubular epithelial
cells, macrophages and myofibroblasts and molecules regulating their
behavior.
List of
Selected Publications (Requires Acrobat
Reader)
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