Short CV/Education and training

  • 1985 – 1991
    Studied medicine at Damascus University, Syria

  • 1992
    Permission to continue medical training in the USA (ECFMG Certification)

  • 1993 – 1996
    Abington Memorial Hospital, Abington, PA, USA, residency in internal medicine

  • 1996
    Specialist in internal medicine in the USA, American Board of Internal Medicine; board certification in internal medicine

  • 1996 – 2000
    Yale University School of Medicine, New Haven, CT, USA: fellowship in endocrinology, diabetes and metabolism; afterward associate research scientist

  • 1998
    Additional qualification in the USA; American Board of Internal Medicine: board certification in the subspecialty of endocrinology, diabetes and metabolism

  • 2000 – 2003
    Doctor at the University Medical Centre Mannheim, Germany

  • 2001
    Licence to practise medicine from the Regional Council in Stuttgart, Germany

  • 2001
    Specialist in internal medicine, State Medical Chamber of Baden-Württemberg, Germany

  • 2002
    Additional specialisation as endocrinologist, State Medical Chamber of Baden-Württemberg

  • 2003
    Additional specialisation as gastroenterologist, State Medical Chamber of Baden-Württemberg

  • 2003
    Certification "Diabetologist DDG", German Diabetes Association (DDG)

  • 2004
    Research associate at the Max Planck Institute of Biochemistry, Martinsried, Germany

  • Since 2005
    Group leader at the Max Planck Institute of Biochemistry and at Heidelberg University, Germany

  • 2010
    Professor by special appointment, Heidelberg University

Selected publications

  • Bentmann, A. et al.: Circulating fibronectin affects bone matrix, whereas osteoblast fibronectin modulates osteoblast function. In: J Bone Miner Res, 2010 Apr; 25(4). S. 706-715.

  • Kawelke, N. et al.: Isoform of fibronectin mediates bone loss in patients with primary biliary cirrhosis by suppressing bone formation. In: J Bone Miner Res., 2008 Aug; 23(8). S. 1278-1286.

  • Nakchbandi, I.A. et al.: Circulating levels of interleukin-6 soluble receptor predict rates of bone loss in patients with primary hyperparathyroidism. In: J Clin Endocrinol Metab., 2002 Nov; 87(11). S. 4946-4951.

  • Nakchbandi, I.A. et al.: Parathyroid hormone-related protein induces spontaneous osteoclast formation via a paracrine cascade. In: Proc Natl Acad Sci USA., 2000 Jun 20; 97(13). S. 7296-7300.

Complete list of publications

Selected projects

  • The focus of our laboratory is on the role of the extracellular matrix and its interaction with the surrounding cells in normal physiology and in the case of various diseases. This can be divided into two main parts: 1) the role of the matrix itself and 2) the function of the cells' matrix receptors.

Liver diseases:

  • Our group was able to show for the first time that patients with chronic cholestatic liver diseases have an increase in isoforms of fibronectin. We were also able to determine that one isoform of fibronectin (namely, the oncofoetal isoform) has a role in the secondary osteoporosis associated with these diseases (Kawelke et al. Kawelke et al.) (see below, under osteoporosis). Furthermore, we were able to confirm that it is possible to predict the degree of fibrosis that will occur in one-third of patients with a chronic hepatitis C infection, because the fibronectin isoforms are affected in those patients ( Hackl et al.). Based on the above-mentioned work, we have begun to research the effects of deactivating fibronectin in stellate cells. Mice that were unable to produce fibronectin in their stellate cells exhibited, without additional stimulation, a clear increase in fibrosis, which was initially very surprising (Figure). This suggests that stellate cells are overstimulated in the absence of fibronectin. We assume that fibronectin is necessary for TGF-beta production and storage. Additional work in this area includes research on fibrosis in mice who produce a mutated form of fibronectin that cannot interact with RGD-binding integrins. We also want to investigate whether a peptide that inhibits the binding of fibronectin with collagen can reverse fibrosis. Due to the central roll of [beta]1-integrin, we are also investigating the influence of integrins that contain [beta]1, both in vitro and in vivo.

Kidney diseases:

  • Previous work has shown that injected fibronectin makes its way via blood circulation to the kidneys and is deposited in the mesangial matrix of the glomeruli. Based on the above-mentioned work, we have begun to research the effects of deactivating fibronectin in the bloodstream and in mesangial cells. We were able to induce diabetes mellitus in conditional knockout mice in which both plasma fibronectin and mesangial cell fibronectin had been deactivated. The deactivation of fibronectin resulted in a reduced expansion of the mesangial matrix as well as the reduced mortality of the animals. Interestingly, the plasma fibronectin alone seemed to be responsible for roughly one-third of the expansion of the mesangium. Additional work in this area is concerned with the interaction of mesangial cells and the surrounding matrix and the influence of hyperglycaemia on the properties of fibronectin matrix assembly. The interaction of the fibronectin deposited in the kidneys on the behaviour of the mesangial cells will continue to be an area of further research. It is our goal to understand the influence of diabetes on matrix assembly and to use this understanding to develop new therapeutic approaches.

Tumour diseases:

  • Breast and prostate cancer tumour cells often form metastases in bone marrow. It is suspected that the tumour cells modify already present physiological stem cell niches according to their own needs. Two niches in the bone marrow have been identified that foster the growth of haematopoietic stem cells and that may also be used by tumour cells in different ways. A distinction is made between the vascular niche, which is located in the area of the sinusoidal blood vessels, and the osteoblastic niche, which is located at the boundary between bone and bone marrow. In this way, bone marrow could function as a type of pre-metastastic niche in the case of breast or prostate cancer. New finding show that tumour cell-specific factors prepare removed tissue for colonisation by tumour cells. In the process, there is an increase in fibronectin expression in the area of the pre-metastastic niche. Fibronectin repression in the vascular niche resulted in the slowing of tumour growth, which was itself a result of reduced angiogenesis. In contrast, osteoblast-specific fibronectin deletion affected only the early developmental stage of the tumours. On the one hand, these observations could be explained by the reduced functionality of the osteoblasts in the absence of fibronectin, but on the other, the influence could be the result of the missing osteoblast-specific fibronectin isoforms that increase the cell adhesion, proliferation and motility of tumour cells. One-third of the animals in which metastases had been induced exhibited a spontaneous regression of the tumours, without any other medical intervention occurring. The spontaneous regression was age-dependent and appeared 8 to 17 weeks after the application of the tumour cells. The complete regression of the osteolytic bone lesions was connected to the healing process for the bone tissue, which expressed itself in densification of the bone. Additional research is concerned with the role of fibronectin in the implantation of tumour cells in metastatic niches ("homing"). The use of proteome analyses (via SILAC technology) should provide evidence of how the early stages of tumour cell implantation in bone marrow can be affected. Research into immune response in the absence of fibronectin should provide information on the reasons why one-fourth of the tumours exhibited complete regression.


  • Our group was able to determine for the first time that one of the isoforms of fibronectin (namely, the oncofoetal isoform) is involved in secondary osteoporosis, which is caused by chronic cholestatic liver disease. We investigated the hypothesis that, in chronic cholestatic liver diseases, fibronectin isoforms make their way into the bloodstream from the activated stellate cells in the liver and in this way affect bone-forming cells (osteoblasts). It turned out to actually be the case that patients exhibit higher levels of isoforms circulating in the bloodstream than healthy subjects and that the oncofoetal isoform of fibronectin correlates negatively with osteocalcin, a bone-formation marker. in vitro and in vivo experiments have confirmed a causal relationship. For example, injecting the isoform into mice led to bone-formation being inhibited and to a loss of bone ( Kawelke et al.). Additional work has shown that O-glycosylation in the variable region of fibronectin is responsible. We are planning to identifiy the receptors involved and to modify our new findings accordingly, in order to positively influence bone-formation.

Skeletal development:

  • Working together with M. Moser and A. Aszodi at the Max Planck Institute of Biochemistry, we are investigating the effects on bones of various modifications in the integrin signalling pathway within bone-forming cells, the osteoblasts. Thus, the deactivation of [beta]1-integrin in the osteoblasts leads to changes in the bones (Phillips et al.). In addition, we are investigating the role of the Kindlin molecules and various GTPases in different type of cells in bones.

Additional qualifications

  • Internal medicine (USA, Germany)

  • Endocrinology and diabetology (USA, Germany)

  • Gastroenterology (Germany)


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