Christiana Ruhrberg

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Christiana Ruhrberg
Christiana Ruhrberg (2024).jpg
Scientific career
Institutions University College London
Thesis Envoplakin and periplakin, novel components of the cornified envelope and desmosomes.  (1997)

Christiana Ruhrberg is a German-British cell biologist who is Professor of Neuronal and Vascular Biology. University College London [1] She investigates how cells interact during the development of mammals and examines how similar interactions influence the repair and regeneration of adult organs.

Contents

Early life and education

Ruhrberg was an undergraduate student at the Justus-Liebig-Universitaet, where she majored in biology. [2] She was a Master's student at the University of Sussex, where she investigated genetic changes in ovarian cancer. [2] Ruhrberg moved to the Imperial Cancer Research Fund to define the genomic organisation in the human surfeit locus. [2] Ruhrberg was a doctoral researcher at the Imperial Cancer Research Fund, where she worked under the supervision of Fiona Watt. [3] [4] In 1986, the British Society for Cell Biology named her Young Cell Biologist of the Year. She received her PhD from Imperial College London in 1997. Ruhrberg was a postdoctoral researcher at the National Institute for Health Research, where she worked under the supervision of Robb Krumlauf to study the development of cranial motor neurons. [5] She returned to the Imperial Cancer Research Fund to work in the laboratory of David Shima, where she investigated molecular mechanisms that underpin the growth of blood vessels. [6]

Research and career

Ruhrberg moved to University College London in 2003, and was promoted to Professor of Neuronal and Vascular Development at UCL in 2011. [2] [7] Here, she has combined her training in neuronal and vascular development to help establish the field of neurovascular co-patterning. [8] [9] She also studies how blood vessels grow in the brain and retina (see selected references).

Awards and honours

Selected publications

Related Research Articles

<span class="mw-page-title-main">Angiogenesis</span> Blood vessel formation, when new vessels emerge from existing vessels

Angiogenesis is the physiological process through which new blood vessels form from pre-existing vessels, formed in the earlier stage of vasculogenesis. Angiogenesis continues the growth of the vasculature mainly by processes of sprouting and splitting, but processes such as coalescent angiogenesis, vessel elongation and vessel cooption also play a role. Vasculogenesis is the embryonic formation of endothelial cells from mesoderm cell precursors, and from neovascularization, although discussions are not always precise. The first vessels in the developing embryo form through vasculogenesis, after which angiogenesis is responsible for most, if not all, blood vessel growth during development and in disease.

<span class="mw-page-title-main">Pericyte</span> Cells associated with capillary linings

Pericytes are multi-functional mural cells of the microcirculation that wrap around the endothelial cells that line the capillaries throughout the body. Pericytes are embedded in the basement membrane of blood capillaries, where they communicate with endothelial cells by means of both direct physical contact and paracrine signaling. The morphology, distribution, density and molecular fingerprints of pericytes vary between organs and vascular beds. Pericytes help in the maintainenance of homeostatic and hemostatic functions in the brain, where one of the organs is characterized with a higher pericyte coverage, and also sustain the blood–brain barrier. These cells are also a key component of the neurovascular unit, which includes endothelial cells, astrocytes, and neurons. Pericytes have been postulated to regulate capillary blood flow and the clearance and phagocytosis of cellular debris in vitro. Pericytes stabilize and monitor the maturation of endothelial cells by means of direct communication between the cell membrane as well as through paracrine signaling. A deficiency of pericytes in the central nervous system can cause increased permeability of the blood–brain barrier.

Vascular endothelial growth factor, originally known as vascular permeability factor (VPF), is a signal protein produced by many cells that stimulates the formation of blood vessels. To be specific, VEGF is a sub-family of growth factors, the platelet-derived growth factor family of cystine-knot growth factors. They are important signaling proteins involved in both vasculogenesis and angiogenesis.

An angiogenesis inhibitor is a substance that inhibits the growth of new blood vessels (angiogenesis). Some angiogenesis inhibitors are endogenous and a normal part of the body's control and others are obtained exogenously through pharmaceutical drugs or diet.

<span class="mw-page-title-main">Endothelial stem cell</span> Stem cell in bone marrow that gives rise to endothelial cells

Endothelial stem cells (ESCs) are one of three types of stem cells found in bone marrow. They are multipotent, which describes the ability to give rise to many cell types, whereas a pluripotent stem cell can give rise to all types. ESCs have the characteristic properties of a stem cell: self-renewal and differentiation. These parent stem cells, ESCs, give rise to progenitor cells, which are intermediate stem cells that lose potency. Progenitor stem cells are committed to differentiating along a particular cell developmental pathway. ESCs will eventually produce endothelial cells (ECs), which create the thin-walled endothelium that lines the inner surface of blood vessels and lymphatic vessels. The blood vessels include arteries and veins. Endothelial cells can be found throughout the whole vascular system and they also play a vital role in the movement of white blood cells

<span class="mw-page-title-main">Neuropilin</span> Protein receptor active in neurons

Neuropilin is a protein receptor active in neurons.

<span class="mw-page-title-main">VEGF receptor</span> Protein family

VEGF receptors (VEGFRs) are receptors for vascular endothelial growth factor (VEGF). There are three main subtypes of VEGFR, numbered 1, 2 and 3. Depending on alternative splicing, they may be membrane-bound (mbVEGFR) or soluble (sVEGFR).

<span class="mw-page-title-main">VE-cadherin</span> Protein-coding gene in the species Homo sapiens

Cadherin-5, or VE-cadherin, also known as CD144, is a type of cadherin. It is encoded by the human gene CDH5.

<span class="mw-page-title-main">Vascular endothelial growth factor C</span> Growth factor protein found in humans

Vascular endothelial growth factor C (VEGF-C) is a protein that is a member of the platelet-derived growth factor / vascular endothelial growth factor (PDGF/VEGF) family. It is encoded in humans by the VEGFC gene, which is located on chromosome 4q34.

<span class="mw-page-title-main">Periplakin</span> Protein-coding gene in the species Homo sapiens

Periplakin is a protein that in humans is encoded by the PPL gene.

<span class="mw-page-title-main">Envoplakin</span> Protein-coding gene in the species Homo sapiens

Envoplakin is a protein that in humans is encoded by the EVPL gene.

<span class="mw-page-title-main">Vascular endothelial growth factor B</span> Protein-coding gene in the species Homo sapiens

Vascular endothelial growth factor B also known as VEGF-B is a protein that, in humans, is encoded by the VEGF-B gene. VEGF-B is a growth factor that belongs to the vascular endothelial growth factor family, of which VEGF-A is the best-known member.

<span class="mw-page-title-main">Vascular endothelial growth factor A</span> Protein involved in blood vessel growth

Vascular endothelial growth factor A (VEGF-A) is a protein that in humans is encoded by the VEGFA gene.

The lymphatic endothelium refers to a specialized subset of endothelial cells located in the sinus systems of draining lymph nodes. Specifically, these endothelial cells line the branched sinus systems formed by afferent lymphatic vessels, forming a single-cell layer which functions in a variety of critical physiological processes. These lymphatic endothelial cells contribute directly to immune function and response modulation, provide transport selectivity, and demonstrate orchestration of bidirectional signaling cascades. Additionally, lymphatic endothelial cells may be implicated in downstream immune cell development as well as lymphatic organogenesis. Until recently, lymphatic endothelial cells have not been characterized to their optimal potential. This system is very important in the function of continuous removal of interstitial fluid and proteins, while also having a significant function of entry for leukocytes and tumor cells. This leads to further research that is being developed on the relationship between lymphatic endothelium and metastasis of tumor cells . The lymphatic capillaries are described to be blind ended vessels, and they are made up of a single non-fenestrated layer of endothelial cells; The lymph capillaries function to aid in the uptake of fluids, macromolecules, and cells. Although they are generally similar to blood capillaries, the lymph capillaries have distinct structural differences. Lymph capillaries consist of a more wide and irregular lumen, and the endothelium in lymph capillaries is much thinner as well. Their origin has been speculated to vary based on them being dependent on specific tissue environments, and powered by organ-specific signals.(L. Gutierrez-Miranda, K. Yaniv, 2020). A lymph capillary endothelial cell is distinct from other endothelial cells in that collagen fibers are directly attached to its plasma membrane.

Michael Jeltsch is a German-Finnish researcher in the field of Biochemistry. He is an associate professor at the University of Helsinki, Finland. He has more than 70 publications. Jeltsch was the first to show that VEGF-C and VEGF-D are the principal growth factors for the lymphatic vasculature and his research focuses on cancer drug targets and lymphangiogenesis. He has also contributed to other seminal publications in cell biology with transgenesis, protein engineering, recombinant production and purification. In 2006, he developed a synthetic super-VEGF, using a library of VEGF hybrid molecules using a novel, non-random DNA family shuffling method.

Neuroangiogenesis is the coordinated growth of nerves and blood vessels. The nervous and blood vessel systems share guidance cues and cell-surface receptors allowing for this synchronised growth. The term neuroangiogenesis only came into use in 2002 and the process was previously known as neurovascular patterning. The combination of neurogenesis and angiogenesis is an essential part of embryonic development and early life. It is thought to have a role in pathologies such as endometriosis, brain tumors, and Alzheimer's disease.

<span class="mw-page-title-main">Pathophysiology of Parkinson's disease</span> Medical condition

The pathophysiology of Parkinson's disease is death of dopaminergic neurons as a result of changes in biological activity in the brain with respect to Parkinson's disease (PD). There are several proposed mechanisms for neuronal death in PD; however, not all of them are well understood. Five proposed major mechanisms for neuronal death in Parkinson's Disease include protein aggregation in Lewy bodies, disruption of autophagy, changes in cell metabolism or mitochondrial function, neuroinflammation, and blood–brain barrier (BBB) breakdown resulting in vascular leakiness.

<span class="mw-page-title-main">Tumor-associated endothelial cell</span>

Tumor-associated endothelial cells or tumor endothelial cells (TECs) refers to cells lining the tumor-associated blood vessels that control the passage of nutrients into surrounding tumor tissue. Across different cancer types, tumor-associated blood vessels have been discovered to differ significantly from normal blood vessels in morphology, gene expression, and functionality in ways that promote cancer progression. There has been notable interest in developing cancer therapeutics that capitalize on these abnormalities of the tumor-associated endothelium to destroy tumors.

The North American Vascular Biology Organization (NAVBO) is a scientific society promoting knowledge exchange in the area of vascular biology. The society organizes several international scientific meetings annually which broadly cover the areas of development of blood and lymphatic vasculature, cardiovascular and lymphatic disease, vascular matrix biology and vascular bioengineering.

<span class="mw-page-title-main">Neurovascular unit</span>

The neurovascular unit (NVU) comprises the components of the brain that collectively regulate cerebral blood flow in order to deliver the requisite nutrients to activated neurons. The NVU addresses the brain's unique dilemma of having high energy demands yet low energy storage capacity. In order to function properly, the brain must receive substrates for energy metabolism–mainly glucose–in specific areas, quantities, and times. Neurons do not have the same ability as, for example, muscle cells, which can use up their energy reserves and refill them later; therefore, cerebral metabolism must be driven in the moment. The neurovascular unit facilitates this ad hoc delivery and, thus, ensures that neuronal activity can continue seamlessly.

References

  1. "UCL Researcher Profile". 4 October 2024.
  2. 1 2 3 4 5 "Professor Christiana Ruhrberg wins Judah Folkman Award: vision-research.eu – The Gateway to European Vision Research". www.vision-research.eu. Retrieved 28 May 2021.
  3. Ruhrberg, Christiana; Hajibagheri, M.A. Nasser; Parry, David A.D.; Watt, Fiona M. (1997). "Periplakin, a novel component of cornified envelopes and desmosomes that belongs to the plakin family and forms complexes with envoplakin". Journal of Cell Biology. 139 (7): 1835–1849. doi:10.1083/jcb.139.7.1835.
  4. Ruhrberg, C.; Hajibagheri, M. A.; Simon, M.; Dooley, T. P.; Watt, F. M. (1996). "Envoplakin, a novel precursor of the cornified envelope that has homology to desmoplakin". Journal of Cell Biology. 134 (3): 715–729. doi:10.1083/jcb.134.3.715. PMC   2120946 . PMID   8707850.
  5. Gavalas, Anthony; Ruhrberg, Christiana; Livet, Jean; Henderson, Christopher E.; Krumlauf, Robb (2003). "Neuronal defects in the hindbrain of Hoxa1, Hoxb1 and Hoxb2 mutants reflect regulatory interactions among these Hox genes". Development. 130 (23): 5663–5679. doi:10.1242/dev.00802.
  6. Lebrasseur, Nicole (2002). "Branching out requires VEGF". The Journal of Cell Biology. 159 (2): 201. doi:10.1083/jcb1592rr1. PMC   2246537 .
  7. "UCL Profiles". ucl.ac.uk.
  8. Erskine, Lynda; Reijntjes, Susan; Pratt, Thomas; Denti, Laura; Schwarz, Quenten; Vieira, Joaquim M.; Alakakone, Bennett; Shewan, Derryck; Ruhrberg, Christiana (2011). "VEGF signaling through neuropilin 1 guides commissural axon crossing at the optic chiasm". Neuron. 70 (5): 951–965. doi:10.1016/j.neuron.2011.02.052. hdl: 20.500.11820/637f6a4e-2a31-49ab-bfe2-fb2888f3be5b .
  9. Schwarz, Quenten; Gu, Chenghua; Fujisawa, Hajime; Sabelko, Kimberly; Gertsenstein, Marina; Nagy, Andras; Taniguchi, Masahiko; Kolodkin, Alex L.; Ginty, David D.; Shima, David T.; Ruhrberg, Christiana (2004). "Vascular endothelial growth factor controls neuronal migration and cooperates with Sema3A to pattern distinct compartments of the facial nerve". Genes & Development. 18 (22): 2822–2834. doi:10.1101/gad.322904. PMC   528901 .
  10. "Laureats". The Werner-Risau-Prize. Retrieved 28 May 2021.
  11. "The Cheryll Tickle Medal". BSDB – British Society for Developmental Biology. Retrieved 28 May 2021.