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Your search keyword '"Yao, Li-Chin"' showing total 4 results
Start Over Author "Yao, Li-Chin" Topic signal transduction
4 results on '"Yao, Li-Chin"'

1. Pulmonary Lymphangiectasia Resulting From Vascular Endothelial Growth Factor-C Overexpression During a Critical Period

Author

Yao, Li-Chin, Testini, Chiara, Tvorogov, Denis, Anisimov, Andrey, Vargas, Sara O, Baluk, Peter, Pytowski, Bronislaw, Claesson-Welsh, Lena, Alitalo, Kari, and McDonald, Donald M

Subjects
Paediatrics, Biomedical and Clinical Sciences, Lung, Pediatric, Good Health and Well Being, Animals, Female, Humans, Infant, Lung Diseases, Lymphangiectasis, Lymphatic Vessels, Male, Mice, Mice, Inbred Strains, Mice, Transgenic, Pregnancy, Pulmonary Edema, Signal Transduction, Trachea, Uteroglobin, Vascular Endothelial Growth Factor C, Vascular Endothelial Growth Factor Receptor-2, Vascular Endothelial Growth Factor Receptor-3, chylothorax, lung, lymphatic vessels, lymphangiogenesis, lymphangiomatosis, pulmonary, pulmonary edema, VEGFR-2, VEGFR-3, lymphangiomatosis, pulmonary, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

RationaleLymphatic vessels in the respiratory tract normally mature into a functional network during the neonatal period, but under some pathological conditions they can grow as enlarged, dilated sacs that result in the potentially lethal condition of pulmonary lymphangiectasia.ObjectiveWe sought to determine whether overexpression of the lymphangiogenic growth factor (vascular endothelial growth factor-C [VEGF-C]) can promote lymphatic growth and maturation in the respiratory tract. Unexpectedly, perinatal overexpression of VEGF-C in the respiratory epithelium led to a condition resembling human pulmonary lymphangiectasia, a life-threatening disorder of the newborn characterized by respiratory distress and the presence of widely dilated lymphatics.Methods and resultsAdministration of doxycycline to Clara cell secretory protein-reverse tetracycline-controlled transactivator/tetracycline operator-VEGF-C double-transgenic mice during a critical period from embryonic day 15.5 to postnatal day 14 was accompanied by respiratory distress, chylothorax, pulmonary lymphangiectasia, and high mortality. Enlarged sac-like lymphatics were abundant near major airways, pulmonary vessels, and visceral pleura. Side-by-side comparison revealed morphological features similar to pulmonary lymphangiectasia in humans. The condition was milder in mice given doxycycline after age postnatal day 14 and did not develop after postnatal day 35. Mechanistic studies revealed that VEGF recptor (VEGFR)-3 alone drove lymphatic growth in adult mice, but both VEGFR-2 and VEGFR-3 were required for the development of lymphangiectasia in neonates. VEGFR-2/VEGFR-3 heterodimers were more abundant in the dilated lymphatics, consistent with the involvement of both receptors. Despite the dependence of lymphangiectasia on VEGFR-2 and VEGFR-3, the condition was not reversed by blocking both receptors together or by withdrawing VEGF-C.ConclusionsThe findings indicate that VEGF-C overexpression can induce pulmonary lymphangiectasia during a critical period in perinatal development.

Published
2014

2. Schnurri transcription factors from Drosophila and vertebrates can mediate Bmp signaling through a phylogenetically conserved mechanism

Author

Yao, Li-Chin, Blitz, Ira L, Peiffer, Daniel A, Phin, Sopheap, Wang, Ying, Ogata, Souichi, Cho, Ken WY, Arora, Kavita, and Warrior, Rahul

Subjects
Biochemistry and Cell Biology, Genetics, Biological Sciences, 1.1 Normal biological development and functioning, Underpinning research, Generic health relevance, Animals, Base Sequence, Bone Morphogenetic Proteins, Conserved Sequence, DNA-Binding Proteins, Drosophila, Drosophila Proteins, Embryo, Nonmammalian, Gene Expression Regulation, Homeodomain Proteins, Humans, Phylogeny, Response Elements, Signal Transduction, Smad Proteins, Transcription Factors, Vertebrates, Xenopus, Xenopus Proteins, Schnurri, Bone Morphogenetic Protein signaling, Bmp, Smad, transcription, transcriptional activation, transcriptional repression, evolutionary conservation, Medical and Health Sciences, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Bone Morphogenetic Proteins (Bmps) are secreted growth factors that play crucial roles in animal development across the phylogenetic spectrum. Bmp signaling results in the phosphorylation and nuclear translocation of Smads, downstream signal transducers that bind DNA. In Drosophila, the zinc finger protein Schnurri (Shn) plays a key role in signaling by the Bmp2/Bmp4 homolog Decapentaplegic (Dpp), by forming a Shn/Smad repression complex on defined promoter elements in the brinker (brk) gene. Brk is a transcriptional repressor that downregulates Dpp target genes. Thus, brk inhibition by Shn results in the upregulation of Dpp-responsive genes. We present evidence that vertebrate Shn homologs can also mediate Bmp responsiveness through a mechanism similar to Drosophila Shn. We find that a Bmp response element (BRE) from the Xenopus Vent2 promoter drives Dpp-dependent expression in Drosophila. However, in sharp contrast to its activating role in vertebrates, the frog BRE mediates repression in Drosophila. Remarkably, despite these opposite transcriptional polarities, sequence changes that abolish cis-element activity in Drosophila also affect BRE function in Xenopus. These similar cis requirements reflect conservation of trans-acting factors, as human Shn1 (hShn1; HIVEP1) can interact with Smad1/Smad4 and assemble an hShn1/Smad complex on the BRE. Furthermore, both Shn and hShn1 activate the BRE in Xenopus embryos, and both repress brk and rescue embryonic patterning defects in shn mutants. Our results suggest that vertebrate Shn proteins function in Bmp signal transduction, and that Shn proteins recruit coactivators and co-repressors in a context-dependent manner, rather than acting as dedicated activators or repressors.

Published
2006

3. Pulmonary Lymphangiectasia Resulting from Vegf-C Overexpression During a Critical Period

Author

Yao, Li-Chin, Testini, Chiara, Tvorogov, Denis, Anisimov, Andrey, Vargas, Sara O., Baluk, Peter, Pytowski, Bronislaw, Claesson-Welsh, Lena, Alitalo, Kari, and McDonald, Donald M.

Subjects
Lung Diseases, Male, Lymphangiectasis, Vascular Endothelial Growth Factor C, Infant, Mice, Inbred Strains, Mice, Transgenic, Pulmonary Edema, Vascular Endothelial Growth Factor Receptor-3, Vascular Endothelial Growth Factor Receptor-2, Article, Trachea, Mice, Pregnancy, Animals, Humans, Uteroglobin, Female, Lymphatic Vessels, Signal Transduction
Abstract

Lymphatic vessels in the respiratory tract normally mature into a functional network during the neonatal period, but under some pathological conditions they can grow as enlarged, dilated sacs that result in the potentially lethal condition of pulmonary lymphangiectasia.We sought to determine whether overexpression of the lymphangiogenic growth factor (vascular endothelial growth factor-C [VEGF-C]) can promote lymphatic growth and maturation in the respiratory tract. Unexpectedly, perinatal overexpression of VEGF-C in the respiratory epithelium led to a condition resembling human pulmonary lymphangiectasia, a life-threatening disorder of the newborn characterized by respiratory distress and the presence of widely dilated lymphatics.Administration of doxycycline to Clara cell secretory protein-reverse tetracycline-controlled transactivator/tetracycline operator-VEGF-C double-transgenic mice during a critical period from embryonic day 15.5 to postnatal day 14 was accompanied by respiratory distress, chylothorax, pulmonary lymphangiectasia, and high mortality. Enlarged sac-like lymphatics were abundant near major airways, pulmonary vessels, and visceral pleura. Side-by-side comparison revealed morphological features similar to pulmonary lymphangiectasia in humans. The condition was milder in mice given doxycycline after age postnatal day 14 and did not develop after postnatal day 35. Mechanistic studies revealed that VEGF recptor (VEGFR)-3 alone drove lymphatic growth in adult mice, but both VEGFR-2 and VEGFR-3 were required for the development of lymphangiectasia in neonates. VEGFR-2/VEGFR-3 heterodimers were more abundant in the dilated lymphatics, consistent with the involvement of both receptors. Despite the dependence of lymphangiectasia on VEGFR-2 and VEGFR-3, the condition was not reversed by blocking both receptors together or by withdrawing VEGF-C.The findings indicate that VEGF-C overexpression can induce pulmonary lymphangiectasia during a critical period in perinatal development.

Published
2014

4. Pulmonary lymphangiectasia resulting from vascular endothelial growth factor-C overexpression during a critical period

Author

Andrey Anisimov, Sara O. Vargas, Denis Tvorogov, Donald M. McDonald, Lena Claesson-Welsh, Bronislaw Pytowski, Kari Alitalo, Li-Chin Yao, Chiara Testini, Peter Baluk, Yao, Li-Chin, Testini, Chiara, Tvorogov, Denis, Anisimov, Andrey, Vargas, Sara O, Baluk, Peter, Pytowski, Bronislaw, Claesson-Welsh, Lena, Alitalo, Kari, and McDonald, Donald M

Subjects
Lung Diseases, Male, Pathology, Physiology, Vascular Endothelial Growth Factor C, Inbred Strains, Cardiorespiratory Medicine and Haematology, Transgenic, lymphatic vessels, Mice, 0302 clinical medicine, Pregnancy, chylothorax, Uteroglobin, Pediatric, 0303 health sciences, Respiratory distress, Pulmonary edema, 3. Good health, Lymphangiogenesis, Trachea, lymphangiogenesis, medicine.anatomical_structure, Lymphatic system, Vascular endothelial growth factor C, 030220 oncology & carcinogenesis, Respiratory, Female, Cardiology and Cardiovascular Medicine, Signal Transduction, medicine.medical_specialty, Lymphangiectasis, pulmonary, Clinical Sciences, Pulmonary Edema, Biology, lymphangiomatosis, lung, 03 medical and health sciences, medicine, Animals, Humans, 030304 developmental biology, Lung, Infant, medicine.disease, Vascular Endothelial Growth Factor Receptor-3, Vascular Endothelial Growth Factor Receptor-2, VEGFR-3, VEGFR-2, Good Health and Well Being, Cardiovascular System & Hematology, Respiratory epithelium, Respiratory tract
Abstract

Rationale: Lymphatic vessels in the respiratory tract normally mature into a functional network during the neonatal period, but under some pathological conditions they can grow as enlarged, dilated sacs that result in the potentially lethal condition of pulmonary lymphangiectasia. Objective: We sought to determine whether overexpression of the lymphangiogenic growth factor (vascular endothelial growth factor-C [VEGF-C]) can promote lymphatic growth and maturation in the respiratory tract. Unexpectedly, perinatal overexpression of VEGF-C in the respiratory epithelium led to a condition resembling human pulmonary lymphangiectasia, a life-threatening disorder of the newborn characterized by respiratory distress and the presence of widely dilated lymphatics. Methods and Results: Administration of doxycycline to Clara cell secretory protein-reverse tetracycline-controlled transactivator/tetracycline operator-VEGF-C double-transgenic mice during a critical period from embryonic day 15.5 to postnatal day 14 was accompanied by respiratory distress, chylothorax, pulmonary lymphangiectasia, and high mortality. Enlarged sac-like lymphatics were abundant near major airways, pulmonary vessels, and visceral pleura. Side-by-side comparison revealed morphological features similar to pulmonary lymphangiectasia in humans. The condition was milder in mice given doxycycline after age postnatal day 14 and did not develop after postnatal day 35. Mechanistic studies revealed that VEGF recptor (VEGFR)-3 alone drove lymphatic growth in adult mice, but both VEGFR-2 and VEGFR-3 were required for the development of lymphangiectasia in neonates. VEGFR-2/VEGFR-3 heterodimers were more abundant in the dilated lymphatics, consistent with the involvement of both receptors. Despite the dependence of lymphangiectasia on VEGFR-2 and VEGFR-3, the condition was not reversed by blocking both receptors together or by withdrawing VEGF-C. Conclusions: The findings indicate that VEGF-C overexpression can induce pulmonary lymphangiectasia during a critical period in perinatal development.

Published
2014

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