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Article ; Online: Predicting the preclinical efficacy of anti-fibrosis agents using a force-sensing fibrosis on chip system.

Hsia, Isaac / Asmani, Mohammadnabi / Zhao, Ruogang

2023 Volume 228, Page(s) 115194

Abstract: The high attrition rate of drug candidates contributes to the long duration and high cost in modern drug development. A major barrier in drug development is the poor predicting power of the preclinical models. In the current study, a human pulmonary ... ...

Abstract	The high attrition rate of drug candidates contributes to the long duration and high cost in modern drug development. A major barrier in drug development is the poor predicting power of the preclinical models. In the current study, a human pulmonary fibrosis on chip system was developed for the preclinical evaluation of anti-fibrosis drugs. Pulmonary fibrosis is a severe disease characterized by progressive tissue stiffening that leads to respiration failure. To recapitulate the unique biomechanical feature of the fibrotic tissues, we developed flexible micropillars that can serve as in-situ force sensors to detect the changes in the mechanical properties of engineered lung microtissues. Using this system, we modeled the fibrogenesis of the alveolar tissues including the tissue stiffening and the expression of α-smooth muscle actin (α-SMA) and pro-collagen. Two anti-fibrosis drug candidates that are currently under clinical trials (KD025 and BMS-986020) were tested for their potential anti-fibrosis efficacy and the results were compared to those of FDA-approved anti-fibrosis drugs pirfenidone and nintedanib. Both pre-approval drugs were effective in inhibiting transforming growth factor beta 1 (TGF-β1) induced increases in tissue contractile force, stiffness and expressions of fibrotic biomarkers, which are similar to the effects of FDA-approved anti-fibrosis drugs. These results demonstrated the potential utility of the force-sensing fibrosis on chip system in the pre-clinical development of anti-fibrosis drugs.
MeSH term(s)	Humans ; Pulmonary Fibrosis/drug therapy ; Pulmonary Fibrosis/chemically induced ; Pulmonary Fibrosis/metabolism ; Antifibrotic Agents ; Biosensing Techniques ; Lung/pathology ; Transforming Growth Factor beta1 ; Collagen/metabolism ; Fibroblasts
Chemical Substances	Antifibrotic Agents ; Transforming Growth Factor beta1 ; Collagen (9007-34-5)
Language	English
Publishing date	2023-03-06
Publishing country	England
Document type	Journal Article
ZDB-ID	1011023-9
ISSN	1873-4235 ; 0956-5663
ISSN (online)	1873-4235
ISSN	0956-5663
DOI	10.1016/j.bios.2023.115194
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Article ; Online: Fibrosis on a Chip for Screening of Anti-Fibrosis Drugs.

Asmani, Mohammadnabi / Zhao, Ruogang

Methods in molecular biology (Clifton, N.J.)

2021 Volume 2299, Page(s) 263–274

Abstract: Idiopathic pulmonary fibrosis (IPF) is a chronic pathological disorder that targets alveoli interstitial tissues and is characterized by the progressive stiffening of alveolar membrane. The median survival rate of the patients with IPF is less than 5 ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is a chronic pathological disorder that targets alveoli interstitial tissues and is characterized by the progressive stiffening of alveolar membrane. The median survival rate of the patients with IPF is less than 5 years. Currently, IPF has no cure and there are few options to alleviate the progress of this disease. A critical roadblock in developing new anti-fibrosis therapies is the absence of reliable cell based in vitro models that can recapitulate the progressive features of this disease. Here a novel fibrotic microtissue on a chip system is created to model the fibrotic transition of the lung interstitial tissue and the effect of anti-fibrosis drugs on such transitions. This system will not only help to expedite the efficacy analysis of anti-fibrotic therapies but also help to unveil their potential mode of action.
MeSH term(s)	Cells, Cultured ; Drug Evaluation, Preclinical ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Humans ; Idiopathic Pulmonary Fibrosis/drug therapy ; Indoles/pharmacology ; Indoles/therapeutic use ; Lab-On-A-Chip Devices ; Models, Biological ; Pyridones/pharmacology ; Pyridones/therapeutic use
Chemical Substances	Indoles ; Pyridones ; pirfenidone (D7NLD2JX7U) ; nintedanib (G6HRD2P839)
Language	English
Publishing date	2021-05-24
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-1382-5_19
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Article: Cyclic Stretching of Fibrotic Microtissue Array for Evaluation of Anti-Fibrosis Drugs.

Asmani, Mohammadnabi / Kotei, Christopher / Hsia, Isaac / Marecki, Leo / Wang, Tianjiao / Zhou, Chi / Zhao, Ruogang

Cellular and molecular bioengineering

2019 Volume 12, Issue 5, Page(s) 529–540

Abstract: Introduction: Progression of pulmonary fibrosis, characterized by the deterioration of lung tissue's mechanical properties, is affected by respiratory motion-induced dynamic loading. Since the development of anti-fibrosis drugs faces major hurdles in ... ...

Abstract	Introduction: Progression of pulmonary fibrosis, characterized by the deterioration of lung tissue's mechanical properties, is affected by respiratory motion-induced dynamic loading. Since the development of anti-fibrosis drugs faces major hurdles in animal tests and human clinical trials, preclinical models that can recapitulate fibrosis progression under physiologically-relevant cyclic loading hold great promise. However, the integration of these two functions has not been achieved in existing models. Methods: Recently we developed static human lung microtissue arrays that recapitulate the progressive changes in tissue mechanics during lung fibrogenesis. In the current study, we integrate the lung microtissue array with a membrane stretching system to enable dynamic loading to the microtissues. The effects of a pro-fibrotic agent and anti-fibrosis drugs were tested under cyclic stretching. Results: Cyclic stretching that mimics respiratory motion was shown to affect the cytoskeletal organization and cellular orientation in the microtissue and cause the increase in microtissue contractility and stiffness. Fibrosis induction using TGF-β1 further promoted fibrosis-related mechanical activity of the lung microtissues. Using this system, we examined the therapeutic effects of two FDA approved anti-fibrotic drugs. Our results showed that Nintedanib was able to fully inhibit TGF-β1 induced force increase but only partially inhibited stretching induced force increase. In contrast, Pirfenidone was able to fully inhibit both TGF-β1 induced force increase and stretching-induced force increase. Conclusions: Together, these results highlight the pathophysiologically-relevant modeling capability of the current fibrotic microtissue system and demonstrated the potential of this system to be used for anti-fibrosis drug screening.
Language	English
Publishing date	2019-08-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2416037-4
ISSN	1865-5033 ; 1865-5025
ISSN (online)	1865-5033
ISSN	1865-5025
DOI	10.1007/s12195-019-00590-3
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Article ; Online: Bioengineered Skeletal Muscle as a Model of Muscle Aging and Regeneration.

Rajabian, Nika / Shahini, Aref / Asmani, Mohammadnabi / Vydiam, Kalyan / Choudhury, Debanik / Nguyen, Thy / Ikhapoh, Izuagie / Zhao, Ruogang / Lei, Pedro / Andreadis, Stelios T

Tissue engineering. Part A

2020 Volume 27, Issue 1-2, Page(s) 74–86

Abstract: With age, adult skeletal muscle (SkM) is known to decrease in muscle mass, strength, and functional capacity, a state known as sarcopenia. Here we developed ... ...

Abstract	With age, adult skeletal muscle (SkM) is known to decrease in muscle mass, strength, and functional capacity, a state known as sarcopenia. Here we developed an
MeSH term(s)	Aged ; Aging ; Humans ; Muscle Development ; Muscle, Skeletal ; Myoblasts ; Regeneration
Language	English
Publishing date	2020-06-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2420582-5
ISSN	1937-335X ; 1937-3341
ISSN (online)	1937-335X
ISSN	1937-3341
DOI	10.1089/ten.TEA.2020.0005
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Article ; Online: NANOG restores the impaired myogenic differentiation potential of skeletal myoblasts after multiple population doublings

Aref Shahini / Debanik Choudhury / Mohammadnabi Asmani / Ruogang Zhao / Pedro Lei / Stelios T. Andreadis

Stem Cell Research, Vol 26, Iss , Pp 55-

2018 Volume 66

Abstract: Adult skeletal muscle regeneration relies on the activity of satellite cells residing in the skeletal muscle niche. However, systemic and intrinsic factors decrease the myogenic differentiation potential of satellite cells thereby impairing muscle ... ...

Abstract	Adult skeletal muscle regeneration relies on the activity of satellite cells residing in the skeletal muscle niche. However, systemic and intrinsic factors decrease the myogenic differentiation potential of satellite cells thereby impairing muscle regeneration. Here we present data showing that late passage C2C12 myoblasts exhibited significantly impaired myogenic differentiation potential that was accompanied by impaired expression of myogenic regulatory factors (Myf5, MyoD, Myogenin, and MRF4) and members of myocyte enhancer factor 2 family. Notably, ectopic expression of NANOG preserved the morphology and restored the myogenic differentiation capacity of late passage myoblasts, possibly by restoring the expression level of these myogenic factors. Muscle regeneration was effective in 2D cultures and in 3D skeletal microtissues mimicking the skeletal muscle niche. The presence of NANOG was required for at least 15 days to reverse the impaired differentiation potential of myoblasts. However, it was critical to remove NANOG during the process of maturation, as it inhibited myotube formation. Finally, myoblasts that were primed by NANOG maintained their differentiation capacity for 20 days after NANOG withdrawal, suggesting potential epigenetic changes. In conclusion, these results shed light on the potential of NANOG to restore the myogenic differentiation potential of myoblasts, which is impaired after multiple rounds of cellular division, and to reverse the loss of muscle regeneration. Keywords: Aging, Skeletal muscle loss, Sarcopenia, Satellite cells, C2C12 myoblasts, Myogenic differentiation
Keywords	Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2018-01-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: NANOG Restores Contractility of Mesenchymal Stem Cell-Based Senescent Microtissues.

Shahini, Aref / Mistriotis, Panagiotis / Asmani, Mohammadnabi / Zhao, Ruogang / Andreadis, Stelios T

Tissue engineering. Part A

2017 Volume 23, Issue 11-12, Page(s) 535–545

Abstract: Mesenchymal stem cells (MSCs) have been extensively used in the field of tissue engineering as a source of smooth muscle cells (SMCs). However, recent studies showed deficits in the contractile function of SMCs derived from senescent MSCs and there are ... ...

Abstract	Mesenchymal stem cells (MSCs) have been extensively used in the field of tissue engineering as a source of smooth muscle cells (SMCs). However, recent studies showed deficits in the contractile function of SMCs derived from senescent MSCs and there are no available strategies to restore the contractile function that is impaired due to cellular or organismal senescence. In this study, we developed a tetracycline-regulatable system and employed micropost tissue arrays to evaluate the effects of the embryonic transcription factor, NANOG, on the contractility of senescent MSCs. Using this system, we show that expression of NANOG fortified the actin cytoskeleton and restored contractile function that was impaired in senescent MSCs. NANOG increased the expression of smooth muscle α-actin (ACTA2) as well as the contractile force generated by cells in three-dimensional microtissues. Interestingly, NANOG worked together with transforming growth factor-beta1 to further enhance the contractility of senescent microtissues. The effect of NANOG on contractile function was sustained for about 10 days after termination of its expression. Our results show that NANOG could reverse the effects of stem cell senescence and restore the myogenic differentiation potential of senescent MSCs. These findings may enable development of novel strategies to restore the function of senescent cardiovascular and other SMC-containing tissues.
Language	English
Publishing date	2017-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2420582-5
ISSN	1937-335X ; 1937-3341
ISSN (online)	1937-335X
ISSN	1937-3341
DOI	10.1089/ten.TEA.2016.0494
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Article ; Online: NANOG restores the impaired myogenic differentiation potential of skeletal myoblasts after multiple population doublings.

Shahini, Aref / Choudhury, Debanik / Asmani, Mohammadnabi / Zhao, Ruogang / Lei, Pedro / Andreadis, Stelios T

Stem cell research

2017 Volume 26, Page(s) 55–66

Abstract	Adult skeletal muscle regeneration relies on the activity of satellite cells residing in the skeletal muscle niche. However, systemic and intrinsic factors decrease the myogenic differentiation potential of satellite cells thereby impairing muscle regeneration. Here we present data showing that late passage C2C12 myoblasts exhibited significantly impaired myogenic differentiation potential that was accompanied by impaired expression of myogenic regulatory factors (Myf5, MyoD, Myogenin, and MRF4) and members of myocyte enhancer factor 2 family. Notably, ectopic expression of NANOG preserved the morphology and restored the myogenic differentiation capacity of late passage myoblasts, possibly by restoring the expression level of these myogenic factors. Muscle regeneration was effective in 2D cultures and in 3D skeletal microtissues mimicking the skeletal muscle niche. The presence of NANOG was required for at least 15days to reverse the impaired differentiation potential of myoblasts. However, it was critical to remove NANOG during the process of maturation, as it inhibited myotube formation. Finally, myoblasts that were primed by NANOG maintained their differentiation capacity for 20days after NANOG withdrawal, suggesting potential epigenetic changes. In conclusion, these results shed light on the potential of NANOG to restore the myogenic differentiation potential of myoblasts, which is impaired after multiple rounds of cellular division, and to reverse the loss of muscle regeneration.
MeSH term(s)	Animals ; Cell Differentiation ; Cells, Cultured ; Gene Expression Regulation, Developmental ; Mice ; Muscle Development ; Muscle Fibers, Skeletal/cytology ; Muscle Fibers, Skeletal/physiology ; Myoblasts, Skeletal/cytology ; Myoblasts, Skeletal/physiology ; Nanog Homeobox Protein/genetics ; Nanog Homeobox Protein/metabolism ; Regeneration
Chemical Substances	Nanog Homeobox Protein ; Nanog protein, mouse
Language	English
Publishing date	2017-12-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1876-7753
ISSN (online)	1876-7753
DOI	10.1016/j.scr.2017.11.018
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Article ; Online: Fibrotic microtissue array to predict anti-fibrosis drug efficacy

Mohammadnabi Asmani / Sanjana Velumani / Yan Li / Nicole Wawrzyniak / Isaac Hsia / Zhaowei Chen / Boris Hinz / Ruogang Zhao

Nature Communications, Vol 9, Iss 1, Pp 1-

2018 Volume 12

Abstract: A bottleneck in developing new anti-fibrosis therapies is the absence of suitable in vitro models that recapitulate key features of fibrogenesis. Here the authors develop a tissue-on-a-chip model of lung fibrosis and test the therapeutic efficacy of two ... ...

Abstract	A bottleneck in developing new anti-fibrosis therapies is the absence of suitable in vitro models that recapitulate key features of fibrogenesis. Here the authors develop a tissue-on-a-chip model of lung fibrosis and test the therapeutic efficacy of two recent FDA-approved drugs.
Keywords	Science ; Q
Language	English
Publishing date	2018-05-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Fibrotic microtissue array to predict anti-fibrosis drug efficacy

Mohammadnabi Asmani / Sanjana Velumani / Yan Li / Nicole Wawrzyniak / Isaac Hsia / Zhaowei Chen / Boris Hinz / Ruogang Zhao

Nature Communications, Vol 9, Iss 1, Pp 1-

2018 Volume 12

Abstract	A bottleneck in developing new anti-fibrosis therapies is the absence of suitable in vitro models that recapitulate key features of fibrogenesis. Here the authors develop a tissue-on-a-chip model of lung fibrosis and test the therapeutic efficacy of two recent FDA-approved drugs.
Keywords	Science ; Q
Language	English
Publishing date	2018-05-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Fibrotic microtissue array to predict anti-fibrosis drug efficacy.

Asmani, Mohammadnabi / Velumani, Sanjana / Li, Yan / Wawrzyniak, Nicole / Hsia, Isaac / Chen, Zhaowei / Hinz, Boris / Zhao, Ruogang

Nature communications

2018 Volume 9, Issue 1, Page(s) 2066

Abstract: Fibrosis is a severe health problem characterized by progressive stiffening of tissues which causes organ malfunction and failure. A major bottleneck in developing new anti-fibrosis therapies is the lack of in vitro models that recapitulate dynamic ... ...

Abstract	Fibrosis is a severe health problem characterized by progressive stiffening of tissues which causes organ malfunction and failure. A major bottleneck in developing new anti-fibrosis therapies is the lack of in vitro models that recapitulate dynamic changes in tissue mechanics during fibrogenesis. Here we create membranous human lung microtissues to model key biomechanical events occurred during lung fibrogenesis including progressive stiffening and contraction of alveolar tissue, decline in alveolar tissue compliance and traction force-induced bronchial dilation. With these capabilities, we provide proof of principle for using this fibrotic tissue array for multi-parameter, phenotypic analysis of the therapeutic efficacy of two anti-fibrosis drugs recently approved by the FDA. Preventative treatments with Pirfenidone and Nintedanib reduce tissue contractility and prevent tissue stiffening and decline in tissue compliance. In a therapeutic treatment regimen, both drugs restore tissue compliance. These results highlight the pathophysiologically relevant modeling capability of our novel fibrotic microtissue system.
MeSH term(s)	Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Cells, Cultured ; Drug Evaluation, Preclinical/methods ; Fibroblasts ; Fibrosis ; Humans ; Indoles/pharmacology ; Indoles/therapeutic use ; Lung/drug effects ; Lung/pathology ; Lung Compliance/drug effects ; Primary Cell Culture ; Pulmonary Fibrosis/drug therapy ; Pulmonary Fibrosis/pathology ; Pyridones/pharmacology ; Pyridones/therapeutic use ; Tissue Culture Techniques/methods ; Tissue Scaffolds ; Treatment Outcome
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Indoles ; Pyridones ; pirfenidone (D7NLD2JX7U) ; nintedanib (G6HRD2P839)
Language	English
Publishing date	2018-05-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-018-04336-z
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