Person:
Sonntag, Kai-Christian

Profile Picture

Email Address

AA Acceptance Date

Birth Date

Research Projects

Organizational Units

Job Title

Last Name

Sonntag

First Name

Kai-Christian

Name

Sonntag, Kai-Christian
Author's Publications: search.filters.isAuthorOfPublication.fd406d13-714d-4a6f-b18c-dd7ace80acab

Search Results

Now showing 1 - 4 of 4
  • Thumbnail Image
    Publication
    Fast and Efficient Neural Conversion of Human Hematopoietic Cells
    (Elsevier, 2014) Castaño, Julio; Menendez, Pablo; Bruzos-Cidon, Cristina; Straccia, Marco; Sousa, Amaia; Zabaleta, Lorea; Vazquez, Nerea; Zubiarrain, Amaia; Sonntag, Kai-Christian; Ugedo, Luisa; Carvajal-Vergara, Xonia; Canals, Josep Maria; Torrecilla, Maria; Sanchez-Pernaute, Rosario; Giorgetti, Alessandra
    Summary Neurons obtained directly from human somatic cells hold great promise for disease modeling and drug screening. Available protocols rely on overexpression of transcription factors using integrative vectors and are often slow, complex, and inefficient. We report a fast and efficient approach for generating induced neural cells (iNCs) directly from human hematopoietic cells using Sendai virus. Upon SOX2 and c-MYC expression, CD133-positive cord blood cells rapidly adopt a neuroepithelial morphology and exhibit high expansion capacity. Under defined neurogenic culture conditions, they express mature neuronal markers and fire spontaneous action potentials that can be modulated with neurotransmitters. SOX2 and c-MYC are also sufficient to convert peripheral blood mononuclear cells into iNCs. However, the conversion process is less efficient and resulting iNCs have limited expansion capacity and electrophysiological activity upon differentiation. Our study demonstrates rapid and efficient generation of iNCs from hematopoietic cells while underscoring the impact of target cells on conversion efficiency.
  • Thumbnail Image
    Publication
    Molecular Profiles of Parvalbumin-Immunoreactive Neurons in the Superior Temporal Cortex in Schizophrenia
    (Informa Healthcare, 2014) Pietersen, Charmaine Y.; Mauney, Sarah A.; Kim, Susie S.; Passeri, Eleonora; Lim, Maribel P.; Rooney, Robert J.; Goldstein, Jill; Petreyshen, Tracey L.; Seidman, Larry Joel; Shenton, Martha; McCarley, Robert William; Sonntag, Kai-Christian; Woo, Tsung-Ung
    Dysregulation of pyramidal cell network function by the soma- and axon-targeting inhibitory neurons that contain the calcium-binding protein parvalbumin (PV) represents a core pathophysiological feature of schizophrenia. In order to gain insight into the molecular basis of their functional impairment, we used laser capture microdissection (LCM) to isolate PVimmunolabeled neurons from layer 3 of Brodmann’s area 42 of the superior temporal gyrus (STG) from postmortem schizophrenia and normal control brains. We then extracted ribonucleic acid (RNA) from these neurons and determined their messenger RNA (mRNA) expression profile using the Affymetrix platform of microarray technology. Seven hundred thirty-nine mRNA transcripts were found to be differentially expressed in PV neurons in subjects with schizophrenia, including genes associated with WNT (wingless-type), NOTCH, and PGE2 (prostaglandin E2) signaling, in addition to genes that regulate cell cycle and apoptosis. Of these 739 genes, only 89 (12%) were also differentially expressed in pyramidal neurons, as described in the accompanying paper, suggesting that the molecular pathophysiology of schizophrenia appears to be predominantly neuronal type specific. In addition, we identified 15 microRNAs (miRNAs) that were differentially expressed in schizophrenia; enrichment analysis of the predicted targets of these miRNAs included the signaling pathways found by microarray to be dysregulated in schizophrenia. Taken together, findings of this study provide a neurobiological framework within which hypotheses of the molecular mechanisms that underlie the dysfunction of PV neurons in schizophrenia can be generated and experimentally explored and, as such, may ultimately inform the conceptualization of rational targeted molecular intervention for this debilitating disorder.
  • Thumbnail Image
    Publication
    Implementations of Translational Medicine
    (BioMed Central, 2005) Sonntag, Kai-Christian
    New developments in science are rapidly influencing and shaping basic and clinical research and medicine. This has led to the emergence of multiple opportunities and challenges on many levels in the bio-medical and other associated fields. To face these opportunities and challenges, new concepts and strategies are needed. These can be provided by translational research/medicine as an integrative concept based on a multidirectional understanding of research and medicine embedded in a socio-economical environment. Although the implementation of translational research/medicine faces many obstacles, some of its goals have already been part of new programs in local institutions and in medical or scientific societies. These implementations are important in creating a unified national and international system of translational research/medicine.
  • Thumbnail Image
    Publication
    Proteasome Activator Enhances Survival of Huntington's Disease Neuronal Model Cells
    (Public Library of Science, 2007) Seo, Hyemyung; Sonntag, Kai-Christian; Kim, Woori; Cattaneo, Elena; Isacson, Ole
    In patients with Huntington's disease (HD), the proteolytic activity of the ubiquitin proteasome system (UPS) is reduced in the brain and other tissues. The pathological hallmark of HD is the intraneuronal nuclear protein aggregates of mutant huntingtin. We determined how to enhance UPS function and influence catalytic protein degradation and cell survival in HD. Proteasome activators involved in either the ubiquitinated or the non-ubiquitinated proteolysis were overexpressed in HD patients' skin fibroblasts or mutant huntingtin-expressing striatal neurons. Following compromise of the UPS, overexpression of the proteasome activator subunit PA28γ, but not subunit S5a, recovered proteasome function in the HD cells. PA28γ also improved cell viability in mutant huntingtin-expressing striatal neurons exposed to pathological stressors, such as the excitotoxin quinolinic acid and the reversible proteasome inhibitor MG132. These results demonstrate the specific functional enhancements of the UPS that can provide neuroprotection in HD cells.